Original ArticleThe effects of an anxiety sensitivity intervention on insomnia symptoms
Introduction
Symptoms of insomnia disorder, including difficulties initiating or maintaining sleep, are common among the general population, with up to one-third of individuals reporting occasional sleep difficulties [1], [2]. Moreover, approximately 9–15% of the population experience such sleep problems along with daytime dysfunction (e.g., fatigue, irritability, and dysphoric mood; [2]). When sleep problems become chronic and are associated with clinically significant distress and/or impairment, criteria may be met for a diagnosis of insomnia disorder. A formal diagnosis of insomnia disorder may be applicable for about 6% of the population, and these individuals often complain of a wide range of associated problems, including daytime fatigue and dysfunction, increased work absenteeism, problems with concentration and memory, irritability, and poorer quality of life [3]. The prevalence of and disability associated with both elevated levels of insomnia symptoms and insomnia disorder specifically highlight the need for effective treatments for these conditions.
Although effective psychological treatments for insomnia disorder exist (eg, cognitive-behavioral therapy for insomnia (CBT-I); [4]), this type of treatment is often expensive and time-consuming, highlighting the need for less expensive, brief interventions for insomnia disorder and its symptoms. Previous research has examined brief, portable interventions for insomnia disorder (eg, CBT in a brief, online format; [5]), as well as interventions that target insomnia disorder and related anxiety and arousal (eg, mindfulness-based interventions [6]). However, to our knowledge, no studies have yet examined whether a brief intervention targeting a transdiagnostic risk factor relevant for both insomnia and comorbid psychological conditions would reduce symptoms of insomnia.
Anxiety sensitivity (AS) is a transdiagnostic risk factor that has been associated with insomnia symptoms. AS is defined as a fear of physiological arousal associated with anxiety [7]. Individuals with elevated AS fear autonomic arousal because they believe that adverse physical, cognitive, and/or social consequences will arise as a result of this arousal [8]. AS is composed of three dimensions reflecting fears related to physical (eg, fears that one's heart racing is indicative of a heart attack), cognitive (eg, fears that trouble concentrating means one is “going crazy”), and social concerns (ie, fears of publicly observable anxiety symptoms such as blushing; Taylor et al., 2007 [9]). A variety of studies have indicated that AS acts as a risk and maintenance factor for several psychiatric conditions, including various anxiety disorders [10], as well as other conditions, such as depression [11], and eating pathology [12].
Theoretically, AS may affect insomnia symptoms by affecting both nighttime and daytime processes. In terms of nighttime symptoms, the cognitive theory of insomnia highlights how initial sleep difficulty and overarousal at bedtime can become a pattern of recurrent and increasing arousal during subsequent nights, interfering with later sleep attempts [13]. Consistent with this, AS may play a role in contributing to the amplification of anxious arousal [14]; thus, AS may be one factor contributing to overarousal and anxiety at bedtime, resulting in a pattern of sleep difficulties. In addition, the influence of AS on patterns of hyperarousal at bedtime may make individuals with elevated AS more vulnerable to developing chronic insomnia after acute periods of sleep difficulties. Specifically, when attempting to sleep, individuals with elevated AS may be more likely to monitor bodily sensations associated with anxiety and interpret them as harmful, leading to an anxious state of hyperarousal unconducive for sleep. Fitting with this notion, previous studies have found that AS may affect sleep-onset latency. For example, research has demonstrated that elevated AS is predictive of increased sleep-onset latency among individuals with panic disorder [15]. More broadly, Babson, Trainor, Bunaciu, and Feldner (2008) [16] investigated sleep-onset latency among undergraduates and found that AS moderated the relationship between sleep anticipatory anxiety and sleep-onset latency, such that for individuals with elevated AS, sleep anticipatory anxiety was associated with longer sleep-onset latency.
AS may also be related to daytime symptoms and processes related to insomnia symptoms. Here, the cognitive model of insomnia proposes that individuals with insomnia selectively attend to sleep-related threat cues (eg, feelings of fatigue) throughout the day, leading to a distorted perception of a sleep deficit. This in turn may lead to negatively toned cognitive activity, arousal, and distress at bedtime, which, together with dysfunctional beliefs about sleep and sleep-related safety behaviors, form a feedback loop resulting in an actual deficit in sleep [13]. It is possible that AS may play a role in this feedback loop. For example, individuals with high AS, particularly AS cognitive concerns, may be more likely to monitor bodily sensations, such as those associated with sleep difficulties (eg, fatigue, lack of energy, problems in concentration and memory, and decreased alertness; Buysse et al., 2007 [17]), leading to an increased perception of a sleep deficit. In addition, AS may contribute to the interpretation of these sensations as harmful, increasing one's negatively toned cognitive activity, arousal, and distress. Indeed, there is some empirical evidence fitting with this idea. Vincent and Walker found that AS, particularly AS cognitive concerns, predicted sleep-related impairment (2001). These findings may indicate that, throughout the day, individuals with elevated AS notice bodily sensations indicative of a lack of sleep, particularly cognitive sensations, and interpret them as threatening, thus perceiving their sleep problems as more distressing and impairing.
Although more research is needed to determine the exact mechanism accounting for this link between AS and sleep disturbance, the previous literature has consistently shown AS to be associated with insomnia symptoms [15], [16], [18], [19]. As such, targeting AS may lead to reductions in symptoms of insomnia. Fortunately, a parallel line of research has found that AS is malleable through brief cognitive-behavioral interventions. This literature demonstrates that AS can be reduced through brief treatments [20], [21], [22]. More specifically, three randomized controlled trials have tested similar AS interventions consisting of psychoeducation regarding the nature of anxiety and physiological arousal, as well as interoceptive exposure (IE) intended to habituate individuals to feared bodily sensations [23], [24], [25]. These interventions are effective at reducing AS and have also been associated with improved psychological outcomes, such as lowered incidence of Axis I diagnoses, and reductions in suicidality, depression, and anxiety [23], [24], [25].
Despite previous work demonstrating a relationship between AS and insomnia symptoms, as well as research indicating that brief interventions are effective at reducing AS, we are unaware of any prior studies examining whether an AS intervention may reduce insomnia symptoms. Thus, the current study tested the efficacy of a brief AS intervention on insomnia symptoms, compared to a physical health education control condition. We hypothesized that the AS intervention would not have a direct effect on insomnia symptoms because they are not likely to be influenced directly by the intervention condition [26], [27]. However, we hypothesized an indirect effect of the condition such that changes in AS would mediate the relationship between condition and insomnia symptoms one month following the intervention. In addition, we tested these effects for each subscale of AS (ie, physical, cognitive, and social concerns). It was expected that physical and cognitive concerns, but not social concerns, would mediate the relationship between condition and insomnia symptoms. Finally, we hypothesized that these indirect effects would hold after accounting for baseline depressive and anxiety symptoms.
Section snippets
Participants
Participants consisted of 97 individuals recruited from the local community to participate in a larger randomized clinical trial examining the efficacy of a computerized intervention targeting AS, a risk factor associated with anxiety, post-traumatic stress disorder (PTSD), substance use, and suicide. To be eligible for inclusion, participants had to be 18 years of age or older, English speakers, and demonstrate elevated levels of AS cognitive concerns. The exclusion criteria included evidence
Descriptive statistics and correlations
As reported in the efficacy study of the AS intervention previously published on the current sample [24], and as depicted in Fig. 1, 55 participants were assigned to the CAST (treatment) condition and 51 participants were assigned to the PHET (control condition). However, two participants (one each from the CAST and PHET conditions) were not included in the analyses because they did not complete the intervention. An additional seven participants (five from PHET and two from CAST) did not
Discussion
The current study expanded upon previous literature linking AS to insomnia symptoms by investigating the direct and indirect effects of an AS intervention on insomnia symptoms through AS and its subscales. Consistent with prediction, we found an indirect effect of condition mediated by AS such that the AS intervention reduced symptoms of insomnia through reductions in AS. We also found that this indirect effect held when covarying for baseline depressive and anxiety symptoms, providing
Funding sources
This work was in part supported by the Military Suicide Research Consortium (MSRC), an effort supported by the Office of the Assistant Secretary of Defense for Health Affairs under Award No. (W81XWH-10-2-0181). Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the MSRC or the Department of Defense.
Conflict of interest
The authors have no conflicts of interest to disclose.
The ICMJE Uniform Disclosure Form for Potential Conflicts of Interest associated with this article can be viewed by clicking on the following link: http://dx.doi.org/10.1016/j.sleep.2014.11.004.
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2017, Behaviour Research and TherapyCitation Excerpt :The current study also has clinical implications. In extension of prior research (Short et al., 2015), the present study further suggests that CAST + BIAS may have utility for clients suffering from both subclinical and clinically-significant insomnia. While many effective treatments for improving insomnia symptoms exist (e.g., CBT-I), these interventions often target the client's sleep directly and require them to make potentially challenging and temporarily uncomfortable changes to their sleep pattern.