Introduction
As a widespread disease, Insomnia is usually defined as poor sleep or dissatisfaction, accompanied by serious pain, as well as social, interpersonal, and occupational problems [
1‐
4]. With the increasingly fierce social competition, the incidence of insomnia, anxiety and depression of adults was gradually increasing, and the relationships among them were complex [
5].
Insomnia, anxiety, and depression commonly co-occured and were closely related [
5‐
7]. A large number of studies were conducted to explore the association of insomnia with anxiety and depression. A review by Taylor et al. concluded that insomnia was a strong risk factor for depression and anxiety [
8]. Moreover, people with insomnia reported higher levels of anxiety and depression than those without insomnia and were 17.35 and 9.82 times as likely to have clinically significant anxiety and depression, respectively [
9]. Patients with clinical insomnia had a higher risk of developing anxiety and depression than patients without insomnia, which highlighted the importance of insomnia in the development of anxiety and depression [
10,
11]. These studies indicated bad sleep quality may have negative influence on depression and anxiety.
However, evidence also suggested that insomnia was bidirectionally related to anxiety and depression [
7,
9‐
13]. Common-cause hypothesis was proposed to explain the bidirectional relationship between insomnia and anxiety / depression [
14,
15], which hypothesized that insomnia and anxiety/depression were influenced by a common factor, such as neural substrates. According to the common-cause hypothesis, disruption in both anxiety / depression and sleep quality may appear when the common factor alters.
Given the complex relationships between insomnia and anxiety/depression, most of the previous studies are cross-sectional, and the ability to identify causal relationships is limited. More longitudinal studies are needed to confirm the causal relationship between insomnia and psychiatric illnesses [
10,
16,
17]. Moreover, much of the evidence for the relationship is based on clinical samples [
18]. However, relying solely on clinical samples may exaggerate the association of insomnia with anxiety and depression [
19]. Therefore, it is necessary to conduct longitudinal research based on non-clinical samples.
Therefore, in order to overcome the shortcomings in the previous studies mentioned above, we conduct a longitudinal study among non-clinical young Chinese males to investigate whether insomnia predicts the likelihood of future anxiety and depression, and vice versa.
Discussion
The present study selected non-clinical young Chinese males as subjects of the longitudinal study, which could avoid the potential bias of exaggerating the linkages between insomnia, anxiety and depression based on clinical participants [
19]. In our longitudinal study, insomnia was significantly positively related to depression and anxiety both at baseline and follow-up. We further discovered that insomnia at baseline predicted a higher risk of anxious symptoms 8 months later. Our study may suggest a causal relationship between insomnia and anxiety, rather than insomnia and depression.
The prevalence of insomnia, anxiety, and depression at two time points (Table
1.) was consistent with previous studies. Remes and colleagues conducted a systematic review of reviews on the prevalence of anxiety disorders in adult populations, they found the prevalence of anxiety disorders in young adults range from 2.5 to 9.1% [
28]. Sleep disturbances were reported by 30.5% from sample of the UK general population [
29]. 6.7% of 686 male college students suffered from depression in China [
13].
Consistent with previous literatures, the results revealed a significantly positive relationships among insomnia, anxiety, and depression. Prior studies indicated close relationships between insomnia and anxiety/depression. For example, Spoormaker et al. reported a high interrelatedness between sleep and depression/anxiety complaints in 402 non-clinical adults [
30]. João and colleagues utilized regression model to investigate how sleep quality affected mental health in non-clinical population through 2 studies. Their first study showed that sleep quality explained 10.1% and 12.3% of the variances of depression and anxiety, respectively [
18]. Compared with this study, their another research found that sleep quality explained 14.0% and 21.0% of the variances of depression and anxiety, respectively [
31]. Matsumoto et al. reported consistent evidence from 90 Japanese male college students, they found poor sleepers had significantly lower scores in mental component summary (MCS) and higher scores in self-rated depression scale (SDS), indicating sleep problem was closely related to bad mental health conditions [
32]. However, it is worth noting that most studies are cross-sectional and unable to infer causality.
The results of cross-lagged analysis based on our longitudinal data showed that insomnia was a predictive factor of anxiety (Fig.
2B), which indicated there existed a possible causal relationship between insomnia and anxiety. Zou et al. conducted a longitudinal observational study among 686 young Chinese male college students and found that poorer baseline sleep quality predicted a higher risk of anxious symptoms a year later [
13], which was consistent with our results.
Furthermore, we would like to discuss the possible potential mechanisms underlying the predictive effect of insomnia on anxiety. Impaired executive function and dysregulated cortisol may be two neurophysiological mechanisms that may mediate the relationship between sleep disturbance and symptoms of anxiety [
33]. Specifically, sleep loss may impair executive function, which will then diminish the ability to regulate or inhibit symptoms of anxiety. Besides, sleep disturbance may also lead to the dysregulated cortisol, which will contribute to the development of anxiety-related disorder. Consequently, our research suggests a possibility that anxiety can be reduced by enhancing sleep quality in non-clinical young Chinese males.
However, no predictable relationship between insomnia and depression was found in cross-lagged analysis. A potential reason of this result may be that insomnia and depression were influenced by common factor [
14]. Animal studies have provided evidence for the hypothesis that common neural substrates might underlie disturbed sleep and depression [
34,
35]. Moreover, the result may also relate with the scores of depression in T
1 and T
2. As shown in Table
2, no significantly longitudinal change of depression was found in present study.
The whole results of cross-lagged analysis were consistent with the results of a previous cohort study. Neckelmann et al. found that insomnia might be a risk factor for the development of anxiety disorders based on a 11 years interval study, but they did not find evidence suggesting that insomnia would increase the risk of developing depression [
36]. What’s more, another longitudinal study reported that sleep problems in children were proved to be a predictive variable of adulthood anxiety disorders, but not depression disorders [
37]. Similarly, no significant difference of the scores of depression at T
1 and T
2 was found in our study. Moreover, another possible explanation was proposed by researchers. Anxiety disorders were highly comorbid with depression [
5]. Comorbid anxiety might confound the associations between insomnia and depression, namely a confounding effect of the comorbidity of anxiety may occur when the predictive effect of insomnia on the risk of developing depression were explored [
38].
Several limitations should be noted in the present study. First of all, the sample size is relatively small. A larger sample size is needed in the further studies to investigate the relationships between insomnia and mental health problems. Secondly, the subjects of our research are all young males. Since there are gender and age differences in the prevalence of insomnia and mental health problems [
39,
40], the results can’t be generalized to other population. Therefore, we should be cautious when extending our conclusions and further studies could be conducted to explore the relationships based on other population. Third, we didn’t collect demographic information such as region, occupation and so on, future study had better record these data and treat it as confounders in data analysis process. Besides, the attrition rate in the second survey was relatively large, which may limit the generalization of our study. Future researchers need to take action to decrease the subject turnover rate. Finally, although a longitudinal observational study was conducted, we still could not draw solid conclusions about causality. Thus, further randomized block design experiment and intervention studies are needed.
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