Overcoming Insomnia

Profile photo of Chris Irving

Chris Irving


Insomnia can be defined as the subjective difficulty in the initiation or maintenance of sleep, or non-restorative sleep, resulting in significant impairment in daytime functioning (American Psychiatric Association, 2013). Common daytime symptoms of Insomnia include low energy, fatigue, impaired concentration and memory difficulties (Edinger et al., 2004).

Woman covers her face with her hands and green eyes on the grunge backround.

How common is Insomnia?

Acute or short-term Insomnia is very common, with up to 20% of the general population experiencing sleep difficulties on any one night (Staner, 2010). However, once these symptoms have persisted for at least one month, Insomnia becomes classified as chronic, and the prevalence rates drop to about 6% (Staner, 2010).

What impact does it have?

Chronic Insomnia is a debilitating and costly condition, with direct health care costs of Insomnia estimated to be $118.7 million in 2010 in Australia (Economics, 2011).
Indirect factors are an even larger burden for society, with reduced employment levels, lower productivity, higher absenteeism, and higher risk of a motor vehicle or workplace accident as a result of Insomnia accounting for $1.5 billion of costs to Australia in 2010 (Economics, 2011). This higher cost of indirect factors means that Insomnia is being under-treated in Australia.
Insomnia has been shown to be significantly related to a higher risk of both workplace and non-workplace accidents (Kessler et al., 2012), with the average annual costs to government (direct and indirect) found to be 11.9 times higher for individuals with Insomnia than for good sleepers (Daley, Morin, LeBlanc, Gregoire, & Savard, 2009)
If Chronic Insomnia is not treated effectively, it results in a greater risk of mental health problems, with up to 61% meeting criteria for another psychiatric disorder (Stepanski & Rybarczyk, 2006).

Woman with her hands on the grunge backround.  Surreal concept photo manipulation

Insomnia and Depression are highly correlated with each other, with up to 90% of individuals with Major Depressive Disorder (MDD) having sleep quality complaints, and 67% having severe enough sleep disturbances and daytime impairments to meet an additional diagnosis of Insomnia (Franzen & Buysse, 2008). This equates to a 61% higher prevalence rate of Insomnia in MDD than in the general population.

Insomnia is also thought to share other common features with Depression, including low energy, fatigue, decreased motivation, indecisiveness and impaired concentration (Spielman & Anderson, 1999). Consequently, there appears to be a strong relationship between low satisfaction with sleep and poor overall mood (Staner, 2010). However, these sleep disturbances are rarely a focus of intervention in the treatment of Depression.

The definition of a MDD in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has Insomnia listed as a symptom of Depression (American Psychiatric Association, 2013). Because of this definition, mental health clinicians have tended to overlook the course of Insomnia, view it as a secondary condition to Depression, and therefore not worthy of clinical attention (Stepanski & Rybarczyk, 2006). However, for the Insomnia to be truly secondary to Depression, it must have begun with the onset of the depressive episode, and remit once the MDD does. As soon as the course of Insomnia differs to that of an individual’s Depression, a co-morbidity of MDD and Insomnia is present, and an additional diagnosis of Insomnia should be given (American Psychiatric Association, 2013).


Insomnia has an earlier average age of onset in comparison to Depression.
Between 40-69% of individuals with Depression reported that their Insomnia appeared before any other depressive symptoms (Franzen & Buysse, 2008; Johnson, Roth, & Breslau, 2006).
Eight epidemiological studies have identified that Insomnia at baseline significantly increased the risk of developing MDD by follow-up 1-3 years later (Riemann & Voderholzer, 2003).
If an Insomnia episode remained for longer than 2 weeks, there was nearly a 50% chance of developing MDD at a later date (Buysse et al., 2008).
Whilst prior Insomnia was found to be significantly associated with the onset of MDD, Depression was not significantly associated with the future onset of Insomnia (Johnson et al., 2006).
Even if Insomnia was initially secondary to Depression, once it remains for one month it is likely to have developed into a separate and chronic problem. This is due to the poor sleeping practices, daytime habits, and unhelpful beliefs about sleep that people develop over time in an attempt to overcome their Insomnia. These perpetuating factors may include excessive time in bed awake, high caffeine during the day or alcohol usage at night, napping during the day, excessive focus on and worry about sleep, and conditioned hyper-arousal at night (Yang et al., 2006). Unless these perpetuating factors are specifically targeted through treatment for Insomnia, it is unlikely that sleep complaints will improve (Carney, Harris, Freedman & Segal, 2011).

Untreated Insomnia increases both the severity and duration of Depression (Staner, 2010). Furthermore, if Insomnia remains after Depression has remitted, the chance of a MDD relapse is much higher. Research indicates that 40% of individuals with Depression will relapse within a ten month period (Paykel, 2008). Of all the 21-items on the Beck Depression Inventory, sleep difficulties were the only symptom that significantly predicted a depressive relapse over the 4-week period following remission (Perlis, Giles, Buysse, Tu, & Kupfer, 1997). Chronic insomnia must therefore be targeted alongside MDD when the conditions co-exist for optimal treatment outcomes.


When Depression and Chronic Insomnia occur together and vary in their course, it is important to target them both in an effective treatment intervention. Medical practitioners appear to administer antidepressants and hypnotics over psychological treatments because they are more easily accessible, quick to administer, and offer lower initial and short-term costs (Economics, 2011). They are also more likely to favour pharmacological over non-pharmacological interventions due to the traditional biomedical model of training in these facilities, which minimises the psychological and social factors involved in mental health disorders (Frostholm et al., 2005). Consequently, antidepressants are the most common treatment for Depression (McManus, Mant, Mitchell, Britt, & Dudley, 2003), and hypnotics are the most common treatment for Insomnia (Charles et al., 2009).

Hypnotics have been found to improve sleep in individuals with Depression alongside antidepressant treatment (Asnis et al., 1999). Another large study recruited 545 patients with a diagnosis of both Insomnia and Depression, and found significant improvements in sleep efficiency, sleep quality, and total sleep time after both four and eight weeks in a combined antidepressant and hypnotic treatment when compared to an antidepressant plus placebo treatment (Fava et al., 2006). Importantly, Depression improvements were also significantly greater at both week 4 and week 8 (p < .01). Therefore, when co-morbidities exist, specifically treating both Insomnia and Depression can result in greater amelioration of both conditions.


Several clinical trials have compared the efficacy of hypnotics to non-pharmacological treatments for Insomnia, and have found similar short-term benefits (Riemann & Perlis, 2009). A meta-analysis comparing the two types of treatments across 21 studies found that that cognitive and behavioural therapies for Insomnia had similar efficacy over 4 weeks to hypnotics, with an average effect size of 0.79 vs. 0.80 (Smith et al., 2002). However, the non-pharmacological treatments produced significantly greater reductions in time taken to fall asleep at the beginning of the night, known as sleep onset latency (SOL) (Smith et al., 2002).

CBT-I may be preferable over hypnotics for the treatment of Chronic Insomnia due to its low risk of adverse effects (Smith et al., 2002). It also has greater empirical evidence of long-term sleep benefits, with research showing therapeutic gains maintained or further improved at 1-month, 3- month, 6-month, 1-year, and 2-year follow-up assessments (Morin et al., 2006; Riemann & Perlis, 2009). In contrast, sleep improvements made through hypnotics are rarely retained through long- term treatment (Riemann & Perlis, 2009) and often return to baseline levels of sleep disturbance following the cessation of hypnotic use (Jacobs et al., 2004). Although CBT-I may be seen as an initially expensive treatment, it becomes more cost-effective than GP visits and hypnotic treatment over time due to its greater long-term benefits for Chronic Insomnia (Harsora & Kessmann, 2009). As a result, CBT-I should be more widely used than sleeping pills in the treatment of Chronic Insomnia.

An individual’s belief that they are able to do a task well is known as self-efficacy (Maciejewski, Prigerson, & Mazure, 2000). Increased self-efficacy towards sleep is more likely to occur when an individual with Chronic Insomnia attributes their sleeping improvements to their own behaviour rather than sleeping medication (Harvey, Tang, & Browning, 2005). Because self-efficacy is thought to play a mediating role between stressful life events and Depression severity (Maciejewski et al., 2000), treating Insomnia with CBT-I is likely to have additional positive effects on mood in comparison to hypnotic treatment. This lends further support to the view that CBT-I needs be implemented in the treatment of co-morbid Insomnia and Depression.


Cognitive behavioural therapy for insomnia (CBT- I) is a multi-modal treatment that combines several individual strategies that have been previously developed and utilized in the non-pharmacological treatment of Insomnia (Edinger & Means, 2005). Many of these individual techniques have been shown to be efficacious as stand-alone treatments, including stimulus control (Morin & Azrin, 1987), sleep restriction (Friedman, Bliwise, Yesavage, & Salom, 1991), paradoxical intention (Turner & Ascher, 1979), and progressive muscle relaxation (PMR) (Pendleton & Tasto, 1976). The four main components of CBT-I include:

Psychoeducation about sleep and sleep hygiene recommendations, which helps people to develop more realistic expectations of their sleep and become more aware of factors that can have a negative impact on their sleep.
Sleep Scheduling, which involves stimulus control (helps people to recondition the bed with calmness, sleepiness and sleep instead of spending excessive time awake in bed alert, worried or frustrated) and sleep restriction (helps people to only spend the amount of time in bed that they need for sleep) interventions.
Cognitive therapy, which challenges some of the unhelpful thinking patterns and beliefs about sleep that typically develop in insomnia, such as “I need 8 hours of sleep to function well during the day!”, “I must catch up on lost sleep”, or “If I don’t sleep well tonight, I’ll be ruined for the rest of the week!” These beliefs only increase the anxiety and pressure around sleeping, which makes the Insomnia severity worse over time.
Relaxation techniques, which helps people to lower their stress and arousal levels during the day and before sleep so will find it easier to get to sleep and stay asleep.

The research findings on the efficacy of CBT-I in Primary Insomnia participants suggests superior efficacy for CBT-I over wait-list and placebo controls, as well as PMR, sleep hygiene education, and pharmacological interventions. Meta-analysis found that multi-modal CBT-I produced large effect sizes in both SOL (1.05) and WASO (0.92), and a moderate effect size (0.75) for TST (Morin, Culbert, et al., 1994).

The cumulative findings of the research on CBT-I suggest that it enhances sleep-related self-efficacy, corrects dysfunctional beliefs about sleep, reduces use of sleep medications, improves mood and reduces anxiety symptoms, and leads to long-term functional improvements in both daytime and night-time functioning (Morin et al., 2006). Given such findings, CBT-I can be considered both a highly efficacious and effective treatment for sleep difficulties and related complaints in individuals with Chronic Insomnia. CBT-I is classified as a well-established empirically supported treatment according to the criteria set-forth by the American Academy of Sleep Medicine (Morin et al., 2006).

Once CBT-I’s efficacy was established, varied lengths of treatment as well as forms of administration were assessed. CBT-I remains efficacious even when protocols vary in length from 4 weeks (Edinger et al., 1992) to 8-weeks (Morin et al., 1993), when it is administered individually (Edinger et al., 2001) or in a group setting (Morin et al., 1999), and potentially even when it is self- administered (Rybarczyk, Mack, Harris & Stepanski, 2011), administered with telephone consultation (Mimeault & Morin, 1999), or administered via the Internet (Strom, Pettersson, & Andersson, 2004).


At the time of my Doctoral research, eight studies had investigated the non-pharmacological treatment of Insomnia symptoms in individuals with co-morbid Depression:

The first study administered a six-week self-help sleep program to 57 individuals with Insomnia and Depression (Morawetz, 2003). At post-treatment, the majority of individuals who substantially improved their sleep had also substantially reduced their Depression severity, with 57% reaching depressive remission based on the Beck Depression Inventory scores, and a further 13% achieving at least a 40% reduction in their scores. Interestingly, all individuals who failed to achieve substantial improvements in their sleep also failed to substantially reduce their depression severity (Morawetz, 2003).

The second study assessed six weekly sessions of CBT-I treatment in eight participants with Chronic Insomnia and mild Depression (Taylor, Lichstein, Weinstock, Sanford, & Temple, 2007). They found significant improvements across several sleep measures, which remained significant by the follow-up assessment three months later. Importantly, Depression severity also significantly reduced from pre-treatment to follow-up in all but one participant (Taylor et al., 2007).

A randomized controlled trial (RCT) was then conducted for 30 participants with co-morbid Insomnia and Depression, who were assigned to an SSRI and CBT-I treatment condition or an SSRI and quasi-desensitisation therapy (control) condition for 12 weeks (Manber et al., 2008). The combined treatment group had a 42.3% greater remission rate from Insomnia. A higher remission rate was also found for Depression with CBT-I (61.5%) in comparison to the control therapy (33.3%), but this finding did not reach statistical significance, possibly due to the concurrent commencement of antidepressant therapy in both treatment groups (Manber et al., 2008).

The next RCT recruited 37 individuals with ongoing Insomnia and depressive symptoms following adequate antidepressant treatment, and compared treatment-as-usual plus four weekly sessions of CBT-I to a treatment-as-usual control group (Watanabe et al., 2011). At the eight-week assessment, sleep efficiency, Insomnia severity and Depression severity were all significantly better in the CBT-I group, with 50% reaching remission from their Insomnia compared to 0% of the control group, and 50% reaching remission from their Depression compared to 6% of the control group (Watanabe et al., 2011).

The remaining studies produced promising findings, with CBT-I significantly reducing Insomnia and Depression severity across treatment (Wagley et al., 2012), as well as improving sleep and reducing anxiety (Lancee, van den Bout, van Straten, & Spoormaker, 2013; Maroti, Folkeson, Jansson-Frojmark, & Linton, 2011), lessening suicidal ideation, improving energy, self-esteem, productivity, and well- being (Manber et al., 2011).

Why CBT-I for Co-Morbid Insomnia and Depression?

The rationale for CBT-I treatment in individuals with co-morbid Insomnia and Depression is that the Insomnia is thought to be maintaining a level of Depression through poor satisfaction with sleep and impaired daytime functioning (Franzen & Buysse, 2008; Staner, 2010). Initial antidepressant treatment may improve mood substantially, but its inability to directly address the perpetuating factors of Chronic Insomnia means that gains will often stagnate above the remission threshold in co-morbid cases. By directly targeting the Insomnia with CBT-I at this point, Insomnia is likely to improve, which should subsequently result in additional reductions in Depression severity. As long as a control group is used for comparison, it would then be possible to determine how much of the improvements in Depression could be attributed to the CBT-I intervention.


The RCT that I conducted as part of my Doctoral Thesis examined this very rationale and found that both Depression and Insomnia severity were significantly reduced over four sessions of CBT-I treatment in comparison to a sleep education intervention.
These significant differences were maintained at the 3-month follow-up, and resulted in a ten-times higher long-term remission rate from both conditions through CBT-I.
Reductions in stress and improved sleep hygiene behaviours seemed to be required for CBT-I to produce short-term improvements in Depression severity, whereas cognitive changes seemed to be required for short-term and long-term Insomnia improvements, as well as longer-term improvements in Depression.
Relaxation and behavioural interventions need to be prioritized initially in CBT-I treatment for co-morbid Insomnia and Depression, followed by cognitive interventions for optimal longer-term outcomes.
The cumulative research findings indicate that CBT-I, both on its own, and in addition to antidepressants, is a promising treatment for co-morbid Insomnia and Depression. By optimising the CBT-I intervention for this population and administering it at the right time, significant improvements in sleep and mood are likely to occur, resulting a greater remission rate from both Chronic Insomnia and MDD, and lower risk of relapse into the future, reducing the overall burden of these conditions on society.

Leave a Reply

Your email address will not be published. Required fields are marked *