The COVID-19 pandemic had seriously harmed the mental well-being of people apart from its effect on their physical health; notably, insomnia and disturbed sleep became main health issues globally due to the pandemic [1]. Insomnia, in particular, had grown increasingly common globally among different groups of people during the COVID-19 era [2]. Also, it is commonly documented that those in close contact with the coronavirus had much greater rates of sleep disorder. For example, healthcare workers, especially nurses in COVID-19 care facilities, experienced serious sleeping disorders. Previous research also suggested that COVID-19 patients were more likely to suffer from insomnia compared to persons not infected from the virus [3]. Similarly, the pandemic had worsened sleep problems in immuno-compromised individuals, including cancer patients [4]. Nevertheless, insomnia was not only confined to these particular groups, and many from the general population also struggled with sleep difficulties during the pandemic [5]. This phenomenon, frequently referred to as “COVID-somnia,” profoundly disrupted an individual’s capacity to achieve restorative sleep; thereby, research into the factors influencing the severity of insomnia during the pandamic was necessary [6].

Concerns over viral infections are a leading cause of exacerbating sleep problems. So, this virus-related anxiety might generally be triggered by the concerns, and the ensuing inadequate sleep would compromise immune function and make one more vulnerable to viral infections [7]. Empirical data also indicates that sleep deprivation adversely impacts several facets of the immune function, including decreased natural killer (NK) cell activity, heightened release of inflammatory cytokines, and lower antibody generation post-vaccination. So, ever since these discoveries were made during the COVID-19 outbreak, people had become more worried/anxious about how sleep deprivation lowers immunity and makes people more susceptible to viral infections. The Stress and Anxiety to Viral Epidemics-6 (SAVE-6) scale has been used to measure this anxiety and has been associated with the severity of insomnia by several researchers [8,9]. Nonetheless, the exact processes via which virus-related anxiety influences insomnia and the mediating factors involved in this influence remain insufficiently understood and unclear.

Meanwhile, we analyzed other psychological factors influencing sleep to define the complex interaction between viral anxiety and insomnia severity during the pandemic. The different aspects of the analysis showed that the Glasgow Sleep Effort Scale (GSES) could be used to quantify the obsession with sleep [10]. This scale governs the too much effort expended toward perfect sleep, which might ironically disturb the normal sleep rhythm [11]. In essence, rising anxiety levels demand more effort to fall asleep, thereby maintaining a loop that reduces the quality of sleep [12]. As said earlier, during the pandemic, the idea that loss of sleep might disrupt the immune function and increase the risk of viral infection could elevate anxiety levels. These elevated anxiety levels would more likely induce an increase in sleep effort and lead to higher insomnia severity. Therefore, we postulated that the GSES could control the degree of sleeplessness caused by anxiety.

Metacognition is among the main psychological factors that influence sleep problems. The term “metacognition” describes the psychological processes of monitoring, controlling, and modifying one’s thoughts, focusing on the process rather than the content of the thoughts [13]. Metacognition, as measured by the Metacognitions Questionnaire-Insomnia (MCQ-I) [14], is an important factor to consider in the case of sleep disorders because it keeps intrusive thoughts at bay before bedtime [15]. These intrusive thoughts often include uncontrollable and harmful ideas, such as “Thinking in bed interrupts falling asleep.” Such metacognitive beliefs, also called dysfunctional beliefs, exacerbate hyperarousal and reinforce dysfunctional sleep patterns [16].

Previous research had shown that metacognition might mediate the relationship between viral anxiety and insomnia severity during the COVID-19 pandemic, particularly among healthcare workers [17]. Meanwhile, metacognitive beliefs increased not only among healthcare workers but also in the general population, due to the generally heightened uncertainty and stress, during the pandemic [18]. In addition, studies had shown that metacognitive worry during the pandemic worsened insomnia severity by fueling a vicious cycle of pre-sleep cognitive arousal and intrusive thoughts [19]. So, given this, we aimed to find out the possibility that metacognition in the general population mediates the relationship between pandemic-related anxiety and insomnia severity.

Another important psychological factor that influences insomnia is depression, which should not be overlooked. Depressive symptoms include low mood, lack of interest, and difficulties with daily functioning. The Patient Health Questionnaire-9 (PHQ-9) serves as a self-report assessment for the severity of depressive symptoms [20]. Depression not only acts as a risk factor for insomnia but also mutually strengthens it [21]. Alao, depression can worsen the sleep cycle, as it heightens continuous anxiety, intrusive thoughts, and nocturnal arousal [22].

The COVID-19 pandemic had worsened depression among people by causing social isolation, financial stress, and health-related worries [22]. Depression assessed by PHQ-9 had increased more than threefold during the pandemic, especially among vulnerable social groups [23]. Anxiety related to COVID-19, measured by SAVE-6, was found to be highly associated with depression by causing a negative cognitive arousal [17]. In addition, anxiety aggravates negative thoughts and pessimism about the future, which increases the incidence rate of depression [24]. COVID-19-related anxiety was known to worsen insomnia via depression, especially in healthcare workers who were exposed to anxious circumstances [17]. We propose that depression may serve as a mediating factor in the relationship between pandemic-related anxiety and insomnia severity among the general population. When depressed, anxiety levels rise, making it difficult to fall or stay asleep as the body and mind become overly alert [25]. So, to understand the interplay between anxiety, depression, and insomnia and develop appropriate therapeutic options, the above said relationship must be interpreted.

This study aimed to investigate the links between mental health and sleep by identifying critical factors that impacted insomnia severity during the COVID-19 pandemic. Specifically, we looked into how depression, sleep preoccupation, and sleep-related metacognitive processes influence the connection between viral anxiety and insomnia severity. Based on the results of the study, we proposed the following hypotheses: 1) Viral anxiety contributes to insomnia severity; 2) Psychological factors, including preoccupation with sleep, sleep-related metacognition, and depression, influence the severity of insomnia; and 3) The relationship between SAVE-6 and Insomnia Severity Index (ISI) is mediated by preoccupation with sleep, sleep-related metacognition, and depression.

Table 1 displays the demographics of the 300 generic responders. The sample included an equal number of men and women (n=150, 50.0%), as well as individuals from diverse marital statuses. In terms of psychiatric history, 18.7% (n=56) of the participants said they have previously had depression, anxiety, or insomnia, while 13.0% (n=39) of them said they are now experiencing these disorders or need help with mood management. As for the COVID-19 infection is considered, 62.3% (n=187) of the participants had been infected, while 93.0% (n=279) of them had been vaccinated. Psychological rating scales indicated insomnia severity (ISI: 11.3±5.2), stress and anxiety to viral epidemics (SAVE-6: 12.1±5.2), sleep-related metacognitions (MCQI-14: 34.0±9.3), sleep effort (GSES: 4.3±3.3), and depression (PHQ-9: 5.6±5.2).

Table 2 presents the results of the correlation analysis that showed the correlations between significant factors. ISI correlated with sleep-related metacognitions (MCQI-14: r=0.576, p<0.001), sleep effort (GSES: r=0.612, p<0.001), and depression (PHQ-9: r=0.571, p<0.001), proposing that insomnia severity has strong interactions with sleep-related metacognition, sleep effort, and depression. SAVE-6 positively correlated with sleep-related metacognitions (MCQI-14: r=0.261, p<0.001), sleep effort (GSES: r=0.275, p<0.001), and depression (PHQ-9: r=0.243, p<0.001), implying that viral anxiety (SAVE-6) is associated with sleep-related psychological factors. Additionally, sleep-related metacognitions (MCQI-14), sleep effort (GSES), and depression (PHQ-9) also correlated themselves.

Table 3 shows the results of a linear regression analysis using ISI as the dependent variable and parameters SAVE-6, MCQI-14, GSES, and PHQ-9. The result was statistically relevant, with an adjusted R-square of 0.515 (F=64.48, p<0.001). Among the predictors, MCQI-14 (β=0.132, p<0.001), GSES (β=0.506, p<0.001), and PHQ-9 (β=0.355, p<0.001) were substantially associated with ISI, indicating that higher sleep-related metacognitions, greater sleep effort, and elevated depressive symptoms contribute to increased insomnia severity. In contrast, SAVE-6 (β=-0.070, p=0.118) and age (β=0.019, p=0.173) did not significantly correlate with ISI, suggesting a minimal direct influence of viral anxiety and age on insomnia severity. A separate regression analysis was conducted with SAVE-6 as the dependent variable, with age, ISI, MCQI-14, GSES, and PHQ-9 as predictors. The regression model explained 11.9% of the variance (F=9.06, p<0.001), with age (β=0.053, p=0.003), GSES (β=0.336, p=0.006), and PHQ-9 (β=0.194, p=0.003) as significant predictors. These results suggest that younger age, greater sleep effort, and having depressive symptoms are likely to have higher viral anxiety levels. However, ISI (β=-0.118, p=0.118) and MCQI-14 (β=0.051, p=0.216) did not significantly predict SAVE-6.

Table 4 and Fig. 1 present the results of the mediation analysis examining the relationship between SAVE-6 and ISI, mediated by MCQI-14, GSES, and PHQ-9. The direct effect of viral anxiety (SAVE-6) on insomnia severity (ISI) was not statistically significant (β=-0.060, p=0.171). However, the mediation analysis confirmed the presence of indirect effects, indicating that sleep-related metacognition (MCQI-14), sleep effort (GSES), and depression (PHQ-9) all mediate the relationship between viral anxiety (SAVE-6) and insomnia severity (ISI). Specifically, the indirect impact of MCQI-14 was significant (β=0.07, 95% confidence interval [CI] [0.03, 0.12], p<0.001), pointing out that negative metacognition about sleep contributes to increased insomnia severity in individuals experiencing high viral anxiety. Similarly, the indirect effect of GSES was significant (β=0.09, 95% CI [0.05, 0.14], p<0.001), suggesting that more intense sleep effort leads to severe insomnia among people suffering from high viral anxiety. Furthermore, depression strongly mediated the correlation between viral anxiety and insomnia severity (β=0.09, 95% CI [0.05, 0.14], p<0.001). Further analysis of path coefficients revealed that viral anxiety significantly predicted MCQI-14 (β=0.49, p<0.001), GSES (β=0.18, p<0.001), and PHQ-9 (β=0.25, p<0.001). Similarly, ISI was significantly associated with MCQI-14 (β=0.14, p<0.001), GSES (β=0.48, p<0.001), and PHQ-9 (β=0.34, p<0.001). The total effect of viral anxiety on insomnia severity remained significant (β=0.18, p=0.002), reinforcing the idea that the impact of viral anxiety on insomnia is mediated through cognitive and emotional mechanisms rather than having a direct relationship.

With its adverse consequences, the COVID-19 pandemic has produced unprecedented changes in health behaviors, social relationships, and work-life of both healthcare workers and the general population [32,33]. Studies across diverse populations and cultures have reported increased sleep disturbances and psychological problems attributed to various potential factors, including social confinement, loneliness, economic crisis, and uncertainties about the consequences of the pandemic [5,34]. Previous studies showed that the fear of being infected and of infecting loved ones or colleagues, the rapid deaths of patients, as well as the emotional and physical fatigue produced high rates of stress, anxiety, depression, and insomnia in healthcare workers [1]. This implies the need to conduct studies on the general population as very high rates of insomnia, anxiety, and depression symptoms were prevalent in the general population concerning demographic variations [17,35]. However, exposure to different stressors during the COVID-19 pandemic and their long-term consequences after the pandemic has ceased are yet to be addressed in the general population.

Unlike prior research focusing on the direct effects of pandemic-related stress on sleep, our study highlights the role of psychological mediators—depression, preoccupation with sleep, and sleep-related metacognition—in insomnia severity. Meanwhile, mediation analysis revealed that viral anxiety did not directly influence insomnia severity. However, depression, preoccupation with sleep, and sleep-related metacognition mediated the relationship between viral anxiety and insomnia severity.

Meta-analytic studies and systematic reviews investigating the impacts of COVID-19 clearly revealed that a moderate to large percentage of infected individuals experienced various psychiatric issues, including depression, anxiety, insomnia, PTSD, impaired memory, and so on, both during and after the pandemic [8,36]. Thus, COVID-19-induced anxiety has multifaceted links with stress, depression, worry, panic attacks, and physical symptoms, leading to intrusive thoughts, rumination, and hyperarousal, making it harder to fall asleep [17]. Consistent with these, both viral epidemic-induced anxiety and insomnia severity had significant associations with sleep-related metacognitive awareness, greater sleep effort, and depression levels in the participants of the present study.

However, contrary to our initial prediction, viral anxiety did not exert any direct influence on insomnia severity, as evidenced by the findings of this study. Previous studies suggested that the symptoms of insomnia regarding COVID-19 anxiety could persist both during and after the pandemic [7,37]. This is because COVID-19-induced stressful events trigger episodes of other problems, such as economic uncertainty, financial hardships, and job losses, which might worsen the existing problems like depression, anxiety, and stress, posing a negative impact on cognition, cognitive–emotion regulation, behavioral organization, and mood state, ultimately increasing the risk of chronic insomnia due to increased stressors following the pandemic [17].

In addition, previous studies clearly indicated that health anxiety symptoms measured through different rating scales, such as Generalized Anxiety Disorder [38], Zung’s Self-rating Anxiety Scale [39], and the Depression Anxiety and Stress Scale [22] could not significantly contribute to elevated levels of sleep problems or insomnia while controlling for the effects of other potential factors [19]. Factors including ill coping strategies, worry, and uncertainty about the job and economy after the pandemic ceased were significant contributors to increased sleep disturbances [19,40]. An explanation for this is that not all individuals with viral anxiety ultimately suffer from insomnia. There are individual differences in emotional regulation strategies. Some people have effective coping strategies, such as cognitive reappraisal, which help them manage their anxiety, keeping it from turning into long-term sleep problems [41]. In contrast, individuals with heightened negative effect are more susceptible to sleep disturbances [42]. In other words, the impact of virus-related anxiety on insomnia may vary depending on an individual’s cognitive processing style and emotional regulation abilities, which are reflected in factors identified as significant mediators in this study, such as depression, sleep-related metacognition, and preoccupation with sleep.

The findings of this study help identify other contributing factors to the relationship between viral anxiety and insomnia severity in the COVID-19 pandemic era. In line with this, one of the potential factors was the level of depression and we observed that depression mediated the relationship between viral anxiety and insomnia. The present finding is in agreement with previous research suggesting depression is one of the most significant risk factors for insomnia [43].

Amid the COVID-19 pandemic, restricted social activities, prolonged isolation, and economic crises produced moderate to high levels of depression among a large number of people. The significant life alterations persisted post-pandemic, resulting in enduring psychological discomfort, challenges in emotional regulation, and heightened stress sensitivity—all of which are recognized as factors that elevate the risk of chronic insomnia [44]. In this context, individuals experiencing heightened viral anxiety may exacerbate depressive symptoms, which subsequently heighten vulnerability to chronic insomnia through heightened cognitive and physiological arousal. This indicates that viral anxiety does not directly influence the severity of sleeplessness, but rather functions indirectly through depression as a principal mediator.

In addition to depression, our findings suggest that preoccupation with sleep played a critical role in mediating the relationship between viral anxiety and insomnia severity. During the COVID-19 pandemic, people feared that poor sleep habits could impair their health and negatively affect daytime functioning to cope with work challenges [16]. These cognitive activities and associated action plans produce dysfunctional beliefs, attentional bias, and excessive worry about going to bed preoccupied with getting to sleep quickly along with a firm expectation about sleep needs [16,45]. This excessive cognitive arousal to fall asleep as soon as possible can generate emotional distress, maladaptive beliefs, and fuel intrusive thoughts, impairing the ability to initiate and maintain sleep [16]. Our results confirm this theory by showing that people with high viral anxiety could become unduly preoccupied with sleep loss, therefore limiting relaxing at bedtime and supporting maladaptive sleep patterns. They may have strict sleep expectations (e.g., “I must get exactly 8 hours to function properly”; Harvey [16], 2002), excessive sleep monitoring, or obsessive thoughts about the negative effects of sleep deprivation. Higher sleep effort paradoxically makes insomnia worse, which in turn leads to higher distress and persistent sleep issues. This self-reinforcing cycle is created by the dysfunctional beliefs discussed.

Alongside preoccupation with sleep, sleep-related metacognitive beliefs also played a significant mediating role in the relationship between viral anxiety and insomnia severity. As evidenced in previous research, intrusive thoughts at bedtime occur involuntarily and adversely impact sleep health [14]. During intrusions at bedtime, dysfunctional metacognitive beliefs activate cognitive attentional syndrome, characterized by beliefs concerning the meaning of the intrusions (e.g., thinking in bed prevents me from getting to sleep), as well as strategies aimed at controlling them (e.g., before I fall asleep, I should try to switch off my thoughts) [46]. Sleep-related metacognitive beliefs—such as the belief that one must completely control one’s sleep—intensify nocturnal cognitive arousal, persistent worry, and negative thought cycles, ultimately contributing to the chronicity of insomnia through heightened hyperarousal [15]. Our findings indicate that viral anxiety could exacerbate these maladaptive metacognitive beliefs, making it more difficult for people to disengage from ineffective thought patterns in bed [47]. People who have high degrees of viral anxiety, for instance, may develop rigid sleep-related beliefs, such as the assumption that if they fail to control their thoughts, they will never fall asleep or that perfect sleep regulation is necessary for proper recovery. These maladaptive beliefs heighten sleep-related anxiety, leading to increased sleep control effort, which, unfortunately, exacerbates sleep disruptions. This loop of metacognitive anxiety promotes self-monitoring, whereas negative thinking maintains hyperarousal and prolongs insomnia symptoms [48].

The above findings underline the importance of treating depressive symptoms, excessive sleep effort, and dysfunctional sleep beliefs to break the cycle of chronic insomnia. These conditions can be addressed through several kinds of evidence-based therapy. Cognitive behavioral therapy for insomnia (CBT-I) helps restructure maladaptive sleep-related beliefs and behaviors by promoting healthier sleep patterns through cognitive restructuring and behavioral techniques, like sleep restriction and stimulus control [16]. Metacognitive therapy (MCT) reduces worry by addressing faulty metacognitive ideas about sleep, assisting in the separation from over-monitoring of sleep [49]. Mindfulness-based therapy (MBT) lowers bedtime arousal by encouraging non-judging awareness and acceptance of thoughts, hence reducing sleep preoccupation and anxiety [50].

Given the strong link between pandemic-related stress and sleep disturbances, these interventions should be integrated into digital platforms and community programs to improve accessibility. A combined approach using CBT-I, MCT, and MBT may effectively break the cycle of chronic insomnia, alleviate cognitive-emotional distress, and promote long-term sleep health.

There are several limitations in this study. First, this study’s cross-sectional design limited the ability to detect temporal changes in variables. Therefore, a clear causal link between viral anxiety and insomnia severity was not possible to prove. Future studies should take a longitudinal approach to better comprehend the causal link between these factors over time. Second, self-report measures used in this study might be subjected to response bias, as participants could overstate or understate the prevalence rates. Including objective sleep measurements in future studies could enhance the validity of the findings. Moreover, socio-demographic variations among participants regarding the metacognitive process, sleep effort, and depression have not been examined in the context of viral anxiety and insomnia severity. The findings of the present study are applicable to the general population of Korea in the COVID-19 pandemic era, limiting their generalizability to different countries and cultures. Future research with a more representative sample and appropriate sampling techniques may overcome these limitations.

In conclusion, although viral anxiety does not directly predict insomnia severity, its total effect on sleep disturbances becomes evident when considering the mediating roles of depression, preoccupation with sleep, and metacognition. These psychological processes magnify the effects of viral anxiety, thereby supporting a self-perpetuating loop of hyperarousal, cognitive rumination, and sleep effort, which finally causes chronic insomnia. These findings guide health authorities following the COVID-19 pandemic to develop large-scale, population-based sleep and mental health prevention and intervention programs to assist at-risk individuals and reduce long-term adverse health outcomes. Thus, insomnia is better understood as a result of the combination of metacognition, sleep effort, and depression than as a direct link between viral anxiety and insomnia severity. These findings establish a basis for designing targeted, evidence-based therapies to reduce pandemic-related sleep disturbances and promote long-term sleep health.