Elsevier

Sleep Medicine

Volume 88, December 2021, Pages 180-186
Sleep Medicine

Original Article
Emotion coping strategies and dysfunctional sleep-related beliefs are associated with objective sleep problems in young adults with insomnia

https://doi.org/10.1016/j.sleep.2021.10.014Get rights and content

Highlights

  • Affected sleep in young adults is particularly related to emotion coping strategies and sleep-related beliefs and attitudes.

  • This relation was particularly strong for sleep onset latency and sleep efficiency, but not for total sleep time.

  • Insomnia treatment in young adults should focus more on emotion coping strategies and ideas about sleep.

Abstract

Background

Though insomnia is associated with affected emotion regulation and dysfunctional ideas about sleep, little is known about the relation of these problems with objective sleep disruption. We aimed to explore this relationship in young adults with and without insomnia.

Methods

Twenty young adults with diagnosed insomnia disorder (aged 27.7 ± 8.6 years) and twenty age-matched individuals without insomnia (26.7 ± 7.0 years) completed questionnaires, measuring sleep-related thoughts and emotions and emotion regulation. Objective sleep measurements were collected through 10-days actigraphy as a representative sample of nights, and analyzed for sleep onset latency, sleep efficiency total sleep time. T-tests and multivariate analyses of variance (MANOVA) were conducted for sample characterization and analysis of the association of sleep-related thoughts and emotions and emotion regulation with objective sleep data.

Results

As expected, young people showed more dysfunctional sleep-related thoughts and emotions (all ps ≤ 0.025) and dysfunctional emotion regulation strategies (all ps ≤ 0.040). Surprisingly, MANOVA results showed that only emotion coping strategies after a stressful event (p = 0.017) and dysfunctional beliefs about sleep (p = 0.012), but not other factors of arousal or sleep reactivity, were associated with overall worse sleep, especially sleep onset latency (all ps ≤ 0.012) and sleep efficiency (all ps ≤ 0.010).

Conclusions

Maladaptive emotion coping strategies after a stressful event and dysfunctional sleep-related beliefs and attitudes affect objective sleep onset latency and sleep efficiency in young adults, highlighting the importance of targeting these features in the prevention and treatment of chronic insomnia and improving actual sleep quality.

Introduction

Insomnia disorder is a common sleep disorder affecting about 6–10% of the general population with important health consequences, such as functional impairments, psychological and medical risk, and reduced quality of life [1,2]. Insomnia etiology is however not well understood: a large number of somatic, cognitive and emotional factors seem to play a major role in insomnia [3], but how these factors interfere with actual sleep loss still needs further investigation.

Stress is one of the most important precipitating factors of insomnia [4,5]. Many studies show a significant relationship between major stressful events (eg, family, health, work) and the onset of insomnia [6,7]. However, it seems that the relationship between stress and sleep depends on the type, duration and severity of the stressor [8,9]. Some studies show that individuals with insomnia report a greater frequency of negative life events but also a higher impact of daily stressful events [10,11]. This is further reflected in strong insomnia prevalence increases in the COVID-19 outbreak situation, with many people have developing insomnia in this unprecedented stressful situation of unknown duration [[12], [13], [14]]. Others suggest that chronicity and severity of stress exposure are significant predictors of future sleep disturbance, and that emotional reactivity to stressful events remains the same between younger and older adults, despite the diminished exposure to stressful events with age [8,9].

Insomnia is characterized by heightened levels of physiological, cognitive, and emotional arousal across the 24-h day [4,15], which mediates the relationship between perceived daytime stressors and sleep disturbances [10,[16], [17], [18]]. Indeed, psychosocial or artificial (eg, Trier Social Stress Test, caffeine) stress induces somatic (eg, heart rate), cognitive (eg rumination) and emotional (eg, negative affect) arousal during the day and at bedtime, which disrupts subjective and polysomnographic sleep, through longer sleep onset latency, frequent nocturnal awakenings, shorter sleep duration and lower sleep efficiency [10,16,[19], [20], [21], [22], [23]]. In return, sleep difficulties can influence subsequent emotional and cognitive responses during the next day and night [16,23,24]. More specifically, enhanced cognitive and emotional reactivity, including increased attention to sleep deprivation and its consequences, as well as misconceptions about sleep and harmful compensatory behaviour can further increase physiological arousal which then disrupts sleep, leading to further dysfunctional cognitive and affective activity (rumination, worry) [25,26]. Over time, this cognitive and emotional reactivity perpetuates sleep disturbances and reinforces the vicious circle of insomnia and affected day- and nighttime functioning [4,27,28].

Vulnerability to develop insomnia later in life has also been associated with the presence of several cognitive and emotional factors: pre-sleep cognitive and somatic arousal, rumination, worry, general arousability, neuroticism, negative emotional affect and emotion-oriented coping [[29], [30], [31], [32], [33], [34]]. This notion of vulnerability suggests that premorbid characteristics may contribute to insomnia disorder, including personality traits, sleep reactivity, or emotional and cognitive hyperarousal [30,[35], [36], [37]]. For example, people with insomnia tend to manage stress and conflict through the internalization of emotions and distress [38]. Other studies show that cognitive–emotional arousal negatively influences the relationship between sleep reactivity (lying awake because of arousing events the previous or next day) and stress deregulation [29,30], thus increasing the risk of insomnia's development or its persistence [39]. Similarly, Vgontas and colleagues showed that the phenotype of shorter sleep duration is associated with cognitive-emotional and cortical arousal as well as stress system activation [37].

Other factors such as age further increase the risk of developing insomnia, due to changes in health, circadian rhythm and hormone levels [40]. In adults, total sleep time, sleep efficiency and deep sleep significantly decrease with age, while wake after sleep onset significantly increases with age [41]. However, insomnia features such as stress responsiveness and arousal predisposition seem to affect older people less [9,42,43]. Older adults may be less affected by stress or negative emotions and cognition, perhaps due to habituation and improved stressful coping strategies developed over time [9,43]. These differences in the regulation of emotional and cognitive processes with age must therefore be taken into consideration in order to better understand the mechanisms of insomnia, its natural history and evolution throughout lifetime, and provide customized interventions for insomnia.

Though several studies have thus examined the presence of sleep reactivity and cognitive factors in the development of insomnia [15,27,28], few studies have added objective measures of sleep [28]. Given that insomnia with short sleep duration however typically shows more severe symptoms than insomnia without short sleep duration [44], investigating those factors that influence objective sleep measures might enable us to provide more focused treatment and reduce relapses. Furthermore, most studies investigating factors at play in insomnia either investigate cognitive or emotional factors, not combinations of both. Examining several factors simultaneously in the same sample can provide a more precise and exhaustive description of the profile of individuals with insomnia disorder compared to that of good sleepers. Specific factors are typically investigated in isolation, such as rumination, neuroticism or negative and positive affect. To our knowledge, the association of emotional-cognitive strategies involved in the etiology of insomnia and objective sleep measures, in a young adult population, has not yet been investigated. Results could guide the development of effective early intervention programs to prevent the development of chronic insomnia and its comorbid mental health problems.

The current study thus explores the association between objectively measured sleep difficulties, emotion regulation and sleep-related emotion and cognition in young adults with insomnia disorder, as compared to those without insomnia disorder. Based on previous findings, we hypothesize that: 1) young adults with insomnia disorder will show more comorbid symptoms to insomnia, such as anxiety and depression and arousal levels, but also show more dysfunctional emotion regulation strategies and more dysfunctional sleep-related thoughts and emotions compared to those without insomnia disorder and that 2) higher cognitive arousal levels and sleep reactivity levels will explain differences in sleep onset latency, sleep efficiency and total sleep time more than other emotion-related factors.

Section snippets

Participants

Participants were recruited through local advertising (eg, newspapers) and included after telephone screening [45,46]. Participants were excluded if they had a chronic psychiatric, neurological or other medical condition (including other sleep disorders), were taking psychotropic or hypnotic medication, had done or were doing shift work, were pregnant or lactating, or showed drug or alcohol dependence, except smoking. Participants stopped over-the-counter sleep aids (valerian, herbal

Results

Results of sociodemographic data are presented in Table 1. Groups were equivalent in sample size, age and gender. In line with the definition of insomnia syndrome and its co-morbid symptoms, the insomnia group reported worse quality of sleep (PSQI; p < 0.001; d = 3.12), higher severity of insomnia (ISI; p < 0.001; d = 1.18), more symptoms of depression and anxiety (BAI and BDI; p < 0.001; d = 1.64 and 1.28 respectively) and were more predisposed to increased arousal (APS; p = 0.022; d = 0.77)

Discussion

The results of this study show that maladaptive coping strategies in stressful situations (ie, CISS) and beliefs or attitudes about sleep (ie, DBAS-16) are associated with lower sleep efficiency and longer sleep onset latency in young adults with or without insomnia. The results are contrary to our expectations in insomnia patients. Based on previous findings, we had anticipated a relation with other factors typical of insomnia, such as pre-sleep arousal or sleep reactivity. It underlines the

CrediT authorship contribution statement

All authors are justifiably credited with authorship. Orlane Ballot: Formal analysis, Visualization, Writing - original draft, Writing - review & editing; Yannick Daviaux: Conceptualisation, Investigation, Methodology, Validation, Writing - review & editing; Ernesto Sanz-Arigita: Conceptualization, Investigation, Writing - review & editing; Hans Ivers: Formal analysis, Writing - review & editing; Jean-Arthur Micoulaud-Franchi: Investigation, Writing - review & editing; Stephanie Bioulac:

Funding

This research was supported by LabEx BRAIN (ANR-10-LABX-43). This work was previously presented in poster form at the ESRS Virtual Congress 2020 (September 22–24, 2020).

Acknowledgments

The authors would like to thank Cécile Klochendler for her help in developing and managing the project; Muriel Bacarisse, Cédric Valtat, and Aurelien Boiseau for their help with screening participants and managing the project and students Marie Bromberg, Charly Marteau, Salome Fourmon, Joyce Reesen, Nico Mascaro, Cécile Arrieula, Laura Dahan, Adèle Jacques, and Maxime Kohn for their help in collecting and processing the data.

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