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. 2021 Jul 14;59(4):229–238. doi: 10.2486/indhealth.2020-0251

The relationship among sleep reactivity, job-related stress, and subjective cognitive dysfunction: a cross-sectional study using path analysis

Kuniyoshi TOYOSHIMA 1,*, Takeshi INOUE 2, Akiyoshi SHIMURA 2, Jiro MASUYA 2, Yota FUJIMURA 2,3, Shinji HIGASHI 2,4, Ichiro KUSUMI 1
PMCID: PMC8426552  PMID: 34261824

Abstract

Insomnia, job-related stress, and cognitive dysfunction affect the mental health of workers. However, the relationships among sleep reactivity, job-related stress, and subjective cognitive dysfunction in workers remains not fully understood. Therefore, this study seeks to investigate the relationships among these variables in Japanese adult workers. In total, 536 adult workers in Japan were evaluated using the Japanese version of Ford Insomnia Response to Stress Test, Brief Job Stress Questionnaire, and Cognitive Complaints in Bipolar Disorder Rating Assessment to assess sleep reactivity, job-related stress, and subjective cognitive function, respectively. Path analysis was also carried out. The results of the path analysis showed that sleep reactivity significantly influenced on subjective cognitive dysfunction directly and indirectly via job stressors and stress reaction. Our results may not be generalizable to underage workers because only adult workers were included, which is a limitation of this study. The results of the present study suggest that job-related stress mediates the effect of sleep reactivity on subjective cognitive dysfunction in Japanese adult workers. This underscores the need to evaluate the mediating effect of job-related stress in addressing the subjective cognitive dysfunction associated with insomnia in workers.

Keywords: Sleep reactivity, Job stress, Subjective cognitive function, Mediator, Workers

Introduction

Occupational stress affects the mental health of workers. Mental health problems lead to a loss in work productivity1). Recently, the relationship between cognitive function and presenteeism in workers has attracted much attention. Cognitive dysfunction is considered a cause rather than a consequence of burnout2). The relationship between work-stress-related exhaustion and attention deficit has also been reported3). The relationship between job-related stress and cognitive dysfunction is a close one in workers.

Cognitive functioning can be evaluated objectively and subjectively. Subjective cognitive assessment has the advantage that it can be carried out easily within a short time4). In addition, it has various characteristics and has been found to play important roles in daily life as well as having a correlation with depressive symptoms and quality of life5). In addition, subjective cognitive function is more closely related to social function than objective cognitive function is6). Furthermore, work functioning is associated with subjective cognitive dysfunction7), while psychosocial working conditions affect subjective cognitive dysfunction among employees8). Regarding work productivity, depressive symptoms and subjective cognitive dysfunction affect presenteeism in workers9). Thus, subjective cognitive dysfunction is one of the important factors that influence the mental health of workers.

One of the important factors in workers’ mental health is insomnia. Sleep deprivation affects work performance10), and insomnia has been linked to accidents and work-related errors11). Sleep quality is believed to be affected by job-related stress in workers12). A meta-analysis found a correlation between insomnia and job-related stress among workers13). Furthermore, insomnia is associated with human relationships at the workplace, job satisfaction, and social support status14). Recently, sleep reactivity, the likelihood of sleep disturbances by stressful situations15), has attracted much attention in workers, and this is correlated with depressive and anxiety symptoms16). Simply put, sleep quality is closely associated with job-related stress.

Recent research suggests that insomnia has a correlation with subjective cognitive dysfunction17), and a meta-analysis found a relationship between insomnia and both subjective and objective cognitive dysfunction18). Furthermore, overtime work affects stress responses19). Although, perceived stress decreases subjective cognitive function20), to the best of our knowledge, the effect of insomnia and job-related stress on subjective cognitive dysfunction in workers has not been previously reported.

In particular, we aimed to answer the question of whether stressors and stress reactions mediate the effect of sleep reactivity on subjective cognitive dysfunction. “Sleep reactivity” is considered as “a trait characteristic,” which is consistent over time and across a variety of stress stimuli15, 2123). Regarding subjective cognitive dysfunction, Toyoshima et al suggested the “trait marker –> state marker –> subjective cognitive dysfunction” model24). Therefore, we hypothesized the “trait marker of insomnia –> stress –> cognitive dysfunction” model, referring to the previous studies. Regarding the difference between “sleep quality” and “sleep reactivity,” “sleep quality” is composed of three indicators: falling asleep, staying asleep, and restorative sleep12), whereas “sleep reactivity” is vulnerability to stress-related insomnia, which is a trait characteristic of insomnia25). Regarding the difference between “stressors” and “stress reactions,” “stressors” indicate perceived job stressors, such as perceived job overload, poor physical environment, and interpersonal conflicts, whereas “stress reactions” indicate stress responses, defined by mental and physical symptoms26, 27). Regarding our hypothesis of “sleep reactivity –> stress (stressor, stress reaction) –> subjective cognitive dysfunction,” we referred to the previous model “affective temperaments –> depressive symptoms –> subjective cognitive dysfunction” by Toyoshima et al24). Sleep reactivity is associated with stress-related worry and rumination, cognitive-emotional reactivity, and perceived stress25). “Stress reactions” indicate stress responses, defined by mental and physical symptoms26, 27). Thus, stress-related worry and rumination are considered “stress reactions.” The relationship of sleep reactivity, perceived stress, and stress reaction has been reported. However, the association of sleep reactivity, perceived stress, and stress reaction with subjective cognitive dysfunction is not well understood. Although the relationship of sleep reactivity, stress, and neurobiological dysfunction has been reported23), no studies have reported on the relationship of sleep reactivity, stress (perceived stress and stress reaction), and subjective cognitive dysfunction. Therefore, the present study aimed to investigate the relationships of sleep reactivity, job-related stress, and subjective cognitive dysfunction as well as the mediating role of job-related stress (perceived stress and stress reaction) using a path analysis.

Subjects and Methods

Participants

In total, 597 adult participants were conveniently recruited in Japan between April 2017 and April 2018 in accordance with the Declaration of Helsinki28). The approval from the Local Ethics Committee of Tokyo Medical University was obtained before the commencement of the study (approval number: SH3502). We excluded the participants who were not employed at the time and those who did not complete the assessments in this study. The present study is part of a larger research, where several assessments were evaluated5). Written informed consent was obtained from all the participants before participation. This article does not reveal identifiable information of any of the participant. Recruitment was performed through the word of mouth, using poster at the Tokyo Medical University, and distributing self-administered questionnaires to 597 adult volunteers. Ten participants were currently unemployed, and 51 participants did not complete the assessments. Therefore, the data of 536 participants were used in the analysis.

Self-Assessments

Sleep reactivity

The Ford Insomnia Response to Stress Test (FIRST) evaluates sleep reactivity, that is, the likelihood of sleep disturbances by stressful situations15). It comprises nine items and makes evaluations using the Likert scale from 1 to 4 points. The maximum total score is 36, which indicates extremely high sleep reactivity. In this study, we used the Japanese version (FIRST-J), which was developed and validated on the basis of the original version29).

Job stress

The Brief Job Stress Questionnaire (BJSQ) has been authorized by the Japanese Ministry of Health, Labour and Welfare28) and is considered a standard questionnaire for evaluating occupational stress27). The BJSQ evaluates four areas using a Likert scale: job stressors (with a score range from 17 to 68); stress reaction (with a score range from 29 to 116); social support (with a score range from 9 to 36); and job and life satisfaction (with a score range from 2 to 8). A higher score in the job stressors, stress reaction, and social support shows worse circumstances for each area30), while a higher score in job and life satisfaction shows better circumstances. In the present study, we defined job stressors and stress reaction as “job-related stress.”

Subjective cognitive dysfunction

The Cognitive Complaints in Bipolar Disorder Rating Assessment (COBRA) comprises 16 items and evaluates subjective cognitive dysfunction4). These items are associated with the performance of daily mental tasks4, 31). The COBRA evaluates each item using a four-point scale from 0 to 3. The maximum total score is 48, with a higher score showing worse subjective cognitive dysfunction. In this study, we used the Japanese version, which has been used for the general adult population5, 25, 31).

Statistical analysis

Spearman’s rank correlation analysis using Bonferroni adjustment was used to investigate the relationships among sleep reactivity, job-related stress, and subjective cognitive dysfunction. Multiple regression analyses by forced entry method were conducted using the scores of the COBRA, BJSQ sub-areas, and FIRST-J as dependent variables. Path analysis was conducted to evaluate the effects of sleep reactivity and job-related stress on subjective cognitive dysfunction. We calculated standardized path coefficients to evaluate the degree of the effects. In this study, correlation analysis, multiple regression analysis, and path analysis were performed based on the hypothesis: “trait marker –> stress –> cognitive dysfunction,” namely, “sleep reactivity –> stress –> cognitive dysfunction.” Our previous study reported about “affective temperaments –> depressive symptoms –> cognitive dysfunction,” wherein depressive symptoms partially mediated the relationship between affective temperaments and cognitive dysfunction32). Thus, we assumed that job-related stress might mediate the relationship between sleep reactivity and cognitive dysfunction. Regarding the multiple regression analysis on FIRST-J, the BJSQ scores were not included as independent variables owing to our hypothesis of the path analysis. In addition, regarding the path analysis, only the parameters of sleep reactivity, job-related stress, and subjective cognitive dysfunction were included, owing to our hypothesis of investigating the mediating role of job-related stress in the relationship between sleep reactivity and subjective cognitive dysfunction. These parameters, using path analysis, were analyzed in an exploratory manner based on our hypothesis. All the statistical analyses were conducted using IBM SPSS Statistics for Windows, Version 21.0 (IBM Corp, Armonk, NY, USA), and STATA/MP 16 (StataCorp LLC, College Station, TX, USA), except for path analysis. A path analysis conducted using Mplus version 8.4. A saturated model was used in this study; therefore, a goodness-of-fit index was not mentioned. Results of all analyses yielding p<0.05 were considered statistically significant.

Results

Basic findings

The clinical and sociodemographic characteristics of the research participants are shown in Table 1. All the participants were employed at the time, and 20 (3.7%) individuals had ongoing psychiatric treatment. The five participants were diagnosed as depression, the two participants were diagnosed as anxiety disorder, the six participants were diagnosed as insomnia, the one participant was diagnosed as schizophrenia, none of the participant was diagnosed as bipolar disorder, alcoholism, and drug addiction, and the six participants were diagnosed other psychiatric illness.

Table 1. Basic findings (N=536).

Characteristics Mean (SD) or n (%)
Age (SD) 41.2 (12.0)
Sex (Male) (%) 237 (44.2)
Married (%) 353 (65.9)
Number of cohabiters (SD) 3.0 (1.6)
Years of education (SD) 14.7 (1.8)
Psychiatric history (%) 57 (10.6)
Current psychiatric treatment (%) 20 (3.7)
Drinking (%) 347 (64.7)
Smoking (%) 102 (19.0)
FIRST-J (SD) 19.1 (6.0)
BJSQ sub-areas
 Job stressors (SD) 40.5 (6.2)
 Stress reaction (SD) 53.8 (14.9)
 Social support (SD) 19.0 (5.4)
 Job and life satisfaction (SD) 5.8 (1.4)
COBRA total score (SD) 8.3 (6.5)

Abbreviations: BJSQ, Brief Job Stress Questionnaire; COBRA, Cognitive Complaints in Bipolar Disorder Rating Assessment; FIRST-J, Japanese version of Ford Insomnia Response to Stress Test.

Relationship among sleep reactivity, job-related stress, and subjective cognitive dysfunction

The results of Spearman’s rank correlation analyses are shown in Table 2. There were significantly positive correlations among sleep reactivity and job stressors, stress reaction, social support, and subjective cognitive dysfunction, while there were significantly negative correlations between sleep reactivity and job and life satisfaction. There were significantly positive correlations among subjective cognitive dysfunction and job stressors, stress reaction, and social support, while there were significantly negative correlations between subjective cognitive dysfunction and job and life satisfaction.

Table 2. Spearman’s rank correlation analyses (N=536).

FIRST-J 9–35 -
Job
stressors
20–61 0.17*** -
Stress
reaction
29–112 0.47*** 0.42*** -
Social
support
9–35 0.21*** 0.33*** 0.36*** -
Job and life
satisfaction
2–8 −0.27*** −0.35*** −0.47*** −0.57*** -
COBRA 0–32 0.41*** 0.17** 0.47*** 0.18*** −0.24***

Abbreviations: BJSQ, Brief Job Stress Questionnaire; COBRA, Cognitive Complaints in Bipolar Disorder Rating Assessment; FIRST-J, Japanese version of Ford Insomnia Response to Stress Test.

*p<0.05, **p<0.01, ***p<0.001.

Multiple regression analyses

The results of the multiple regression analyses are shown in Table 3. Significant predictors of subjective cognitive dysfunction were sleep reactivity and stress reaction. Significant predictors of job stressors were marital status, past history of psychiatric illness, current psychiatric treatment, and sleep reactivity. Significant predictors of stress reaction were age, marital status, current psychiatric treatment, and sleep reactivity. Significant predictors of social support were age, marital status, years of education, and sleep reactivity. Significant predictors of job and life satisfaction were marital status, years of education, and sleep reactivity. Significant predictors of sleep reactivity were sex and past history of psychiatric illness.

Table 3. Multiple regression analysis of COBRA, BJSQ, and FIRST (N=536).

COBRA
F (14, 521)
= 12.00,
p<0.0001
Job
stressors
F (10, 525)
= 3.89,
p<0.0001
Stress
reaction
F (10, 525)
= 18.71,
p<0.0001
Social
support
F (10, 525)
= 6.07,
p<0.0001
Job and life
satisfaction
F (10, 525)
= 7.21,
p<0.0001
FIRST-J
F (9, 526)
= 9.04,
p<0.0001
Independent
variables
β VIF β VIF β VIF β VIF β VIF β VIF
Age 0.09 1.51 −0.06 1.45 −0.13** 1.45 0.10* 1.45 0.00 1.45 0.05 1.45
Sex: 1; Male, 2;
Female
0.03 1.31 −0.02 1.31 0.01 1.31 −0.04 1.31 0.00 1.31 0.26*** 1.23
Married status: 1;
No, 2; Yes
−0.04 1.47 −0.11* 1.42 −0.10* 1.42 −0.10* 1.42 0.19*** 1.42 −0.05 1.42
Number of
cohabiters
0.01 1.32 0.07 1.30 −0.01 1.30 −0.08 1.30 0.04 1.30 −0.00 1.30
Years of education 0.03 1.53 −0.09 1.49 −0.04 1.49 −0.17** 1.49 0.14** 1.49 −0.04 1.49
Psychiatric history,
1; No, 2; Yes
0.04 1.32 −0.12* 1.28 0.06 1.28 0.05 1.28 −0.01 1.28 0.15** 1.25
Current psychiatric
treatment, 1; No, 2;
Yes
0.07 1.30 0.13** 1.28 0.09* 1.28 −0.01 1.28 0.00 1.28 0.08 1.27

 

COBRA
F (14, 521)
= 12.00,
p<0.0001
Job
stressors
F (10, 525)
= 3.89,
p<0.0001
Stress
reaction
F (10, 525)
= 18.71,
p<0.0001
Social
support
F (10, 525)
= 6.07,
p<0.0001
Job and life
satisfaction
F (10, 525)
= 7.21,
p<0.0001
FIRST-J
F (9, 526)
= 9.04,
p<0.0001

Drinking, 1; No, 2;
Yes
0.04 1.16 −0.02 1.15 −0.02 1.15 −0.02 1.15 0.01 1.15 −0.00 1.15
Smoking, 1; No, 2;
Yes
−0.03 1.11 −0.02 1.09 −0.01 1.09 −0.08 1.09 −0.03 1.09 0.02 1.09
FIRST-J 0.25*** 1.41 0.17*** 1.15 0.43*** 1.15 0.16*** 1.15 −0.22*** 1.15 - -
BJSQ sub-areas
 Job stressors 0.00 1.35 - - - - - - - - - -
 Stress reaction 0.28*** 1.75 - - - - - - - - - -
 Social support −0.02 1.65 - - - - - - - - - -
 Job and life
satisfaction
−0.04 1.75 - - - - - - - - - -
Adjusted R2 0.22 0.05 0.25 0.09 0.10 0.12

Abbreviations: BJSQ, Brief Job Stress Questionnaire; COBRA, Cognitive Complaints in Bipolar Disorder Rating Assessment; FIRST-J, Japanese version of Ford Insomnia Response to Stress Test; β, standardized regression coefficients; VIF, variance inflation factor.

*p<0.05, **p<0.01, ***p<0.001

Path analysis

We performed path analysis to investigate the relationships among sleep reactivity, job stressors, stress reaction, and subjective cognitive dysfunction (Table 4, Fig. 1). In the model, the squared multiple correlation coefficient of subjective cognitive dysfunction was 0.226.

Table 4. Standardized path coefficients between FIRST-J, job stressors, stress reaction, and COBRA (N=536).

Direct effect to

From Job stressors Stress reaction COBRA

FIRST-J 0.180*** 0.399*** 0.259***
Job stressors 0.347*** 0.005
Stress reaction 0.295***

Indirect effect to

Job stressors Stress reaction COBRA

FIRST-J 0.063*** (via Job stressors) 0.001 (via Job stressors)
0.018** (via Job stressors and Stress reaction)
0.118*** (via Stress reaction)
Job stressors 0.102*** (via Stress reaction)

Total indirect effect to

FIRST-J 0.063*** 0.137***
Job stressors 0.102***

Total effect to

Job stressors Stress reaction COBRA

FIRST-J 0.180*** 0.461*** 0.396***
Job stressors 0.347*** 0.107**
Stress reaction 0.295***

Abbreviations: COBRA, Cognitive Complaints in Bipolar Disorder Rating Assessment; FIRST-J, Japanese version of Ford Insomnia Response to Stress Test.

* p<0.05, ** p<0.01, *** p<0.001

Fig. 1.

Fig. 1.

Path analysis of the FIRST-J, job-related stressors, stress reaction, and the COBRA.

The solid arrows indicate statistically significant paths, and the broken arrow demonstrates non-significant paths. The numbers beside the arrows represent the direct standardized path coefficients. The width of the solid line shows the strength of the effect. The path analysis included only sleep reactivity, job-related stress, and subjective cognitive dysfunction, owing to our hypothesis investigating the mediating role of job-related stress in the relationship between sleep reactivity and subjective cognitive dysfunction. Significant predictors of subjective cognitive dysfunction were sleep reactivity and stress reaction. Significant predictors of job stressors were marital status, past history of psychiatric illness, current psychiatric treatment, and sleep reactivity. Significant predictors of stress reaction were age, marital status, current psychiatric treatment, and sleep reactivity. Significant predictors of social support were age, marital status, years of education, and sleep reactivity. Significant predictors of job and life satisfaction were marital status, years of education, and sleep reactivity. Significant predictors of sleep reactivity were sex and past history of psychiatric illness.

Abbreviations: BJSQ, Brief Job Stress Questionnaire; COBRA, Cognitive Complaints in Bipolar Disorder Rating Assessment; FIRST-J, Japanese version of Ford Insomnia Response to Stress Test, Job stressors; sub-score of job stressors of BJSQ; Stress reaction, sub-score of stress reaction of BJSQ; n.s., not significant.

In the path analysis, sleep reactivity directly affected job stressors (0.180, p<0.001), stress reaction (0.399, p<0.001), and subjective cognitive dysfunction (0.259, p<0.001). Job stressors directly affected stress reaction (0.347, p<0.001), while there was no significant direct effect of job stressors on the subjective cognitive dysfunction (0.005, p=0.914, n.s.). The stress reaction directly affected subjective cognitive dysfunction (0.295, p<0.001).

Sleep reactivity indirectly affected stress reaction via job stressors (0.063, p<0.001), while there was no significant indirect effect of sleep reactivity on subjective cognitive dysfunction via job stressors (0.001, p=0.913, n.s.). Sleep reactivity indirectly affected subjective cognitive dysfunction via job stressors and stress reaction (0.018, p<0.01) and only via stress reaction (0.118, p<0.001). Job stressors affected subjective cognitive dysfunction via stress reaction (0.102, p<0.001). Regarding total indirect effect, sleep reactivity indirectly affected stress reaction (0.063, p<0.001) and subjective cognitive dysfunction (0.137, p<0.001), and job stressors indirectly affected subjective cognitive dysfunction (0.102, p<0.001).

Regarding the total effect, sleep reactivity affected job stressors (0.180, p<0.001), stress reaction (0.461, p<0.001), and subjective cognitive dysfunction (0.396, p<0.001). Job stressors affected stress reaction (0.347, p<0.001) and subjective cognitive dysfunction (0.107, p<0.01). Stress reaction affected subjective cognitive dysfunction (0.295, p<0.001).

To summarize this, the job stressors and stress reaction mediated the influence of sleep reactivity on subjective cognitive dysfunction.

Discussion

The present study shows that sleep reactivity and job-related stress affected subjective cognitive dysfunction, and our path model revealed a rate of 22.6% of subjective cognitive dysfunction in our sample. Furthermore, job-related stress may mediate the influence of sleep reactivity on subjective cognitive dysfunction; however, the indirect effect may be smaller than the direct effect.

Regarding the relationship between sleep reactivity and job-related stress, this study suggests that sleep reactivity may increase the latter. Sleep reactivity is believed to correlate with depressive and anxiety symptoms16). Hence, in the relationship between sleep reactivity and job-related stress, depressive and anxiety symptoms may play important roles in workers. Previous research suggests that insomnia correlates with occupational stress, including human relationships, job satisfaction, and social support status14). In this study, job-related stressors, stress reaction, and poor social support positively correlated with sleep reactivity, whereas having a better job and life satisfaction negatively correlated with sleep reactivity. Our findings suggest that sleep reactivity affects job-related stress, especially stress reaction. Hence, it may be better to consider sleep reactivity in dealing with stress reaction in workers.

Regarding the relationship between job stress and subjective cognitive dysfunction, the present study suggests that strong job stressors and high stress reaction may worsen subjective cognitive dysfunction in workers. Previous research shows that psychosocial working conditions influence subjective cognitive dysfunction8). Our findings suggest that stress reaction may have a stronger effect when compared with job-related stressors on subjective cognitive dysfunction in Japanese workers. In a previous work of research, depressive symptoms were found to affect subjective cognitive dysfunction in workers5). Further, the impact of sleep disturbance and anxiety on cognitive performance has been reported33). Hence, depressive and anxiety symptoms may influence the relationship between stress reaction and subjective cognitive dysfunction.

Regarding the relationship between sleep reactivity and subjective cognitive dysfunction, the results of this study suggests that sleep reactivity may worsen subjective cognitive dysfunction. The relationship between insomnia and subjective cognitive dysfunction has been previously evaluated17, 18), and it is consistent with the results of the present study. Furthermore, the results of this study suggest that sleep reactivity affects subjective cognitive dysfunction via job-related stress in workers. Regarding the mediating role of job-related stress, stress reaction alone exerted a mediating effect, whereas job-related stressors alone exerted no mediating effect but exerted a mediating effect only via stress reaction. One possible reason is that there may be a causal relationship between job-related stressors and stress reaction. That is to say, job-related stressors may be one of the causes of stress reaction at work. However, this study has a cross-sectional design; thus, the causal linkages between the parameters could not be investigated. To the best of our knowledge, the mediator effect of job-related stress in relation to sleep reactivity and subjective cognitive dysfunction in workers is a novel finding. Job-related stress may play some roles in influencing the effect of insomnia on subjective cognitive dysfunction. Sleep reactivity is composed of a genetic component and an environmental component and is considered a genetic vulnerability for developing insomnia34). Therefore, it may be useful to evaluate the mediating effect of job-related stress when workers with high sleep reactivity exhibit subjective cognitive dysfunction.

Considering the impact of subjective cognitive dysfunction on workers, subjective cognitive dysfunction may affect presenteeism directly and mediate the influence of depressive symptoms on presenteeism in workers9). A recent study suggests that parental bonding and resilience affect job-related stress in workers35). Furthermore, job-related stress and sleep disturbance have been reported to affect presenteeism in office workers36). Hence, sleep reactivity and job-related stress should be evaluated along with depressive symptoms when subjective cognitive dysfunction exerts a large effect on presenteeism. In future studies, it is necessary to investigate the role of depressive symptoms in the relationships among sleep reactivity, job stress, and subjective cognitive dysfunction in adult workers.

Limitations

The cross-sectional nature of this study made it impossible to investigate the causal relationships among the variables. Our path model, “sleep reactivity –> stress –> subjective cognitive dysfunction,” could not investigate the modulating role of sleep reactivity, which could also be a limitation of this study. A sample of 536 participants cannot be representative of the entire Japanese workforce. The recruitment was performed at Tokyo; therefore, our study sample was considered “adult workers from the community,” limiting the generalizability of our findings to all Japanese adult workers. That only workers were included precludes the generalization of our results to the general population and individuals with psychiatric disorders. In addition, our results may not be generalizable to underage workers because only adult workers were included. Because all the study participants were recruited in Japan, the results may not be generalizable to other countries. The effects of current medication in this study were also not evaluated. Further, the effects of employment type, working hours, overtime, position, and income were not controlled for. All the assessments were in the form of a subjective questionnaire in this study. The objective sleeping times and objective cognitive functions were also not evaluated in this study. This suggests the need to perform both subjective and objective assessments in studies in the future or even in a follow-up study. Although subjective cognitive dysfunction may affect sleep reactivity or job-related stress, our path analysis could not evaluate it. In addition, the 20 individuals with ongoing psychiatric treatment were evaluated together with healthy individuals in this study; therefore, this heterogeneity in the sample may be a limitation. Although sleep reactivity was evaluated, we did not evaluate the degree of insomnia, which could be another limitation of this study. Finally, the evaluation of subjective cognitive dysfunction was conducted using a scale to measure cognitive dysfunction in mental illness, which is also a limitation of this study.

Conclusions

The results of the present study suggest that sleep reactivity, stressors, and stress reaction may worsen subjective cognitive dysfunction. Although 65% of the effects from sleep reactivity to subjective cognitive dysfunction are direct effects, job-related stress (stressors and stress reaction) mediates the effect of sleep reactivity on subjective cognitive dysfunction. Hence, this suggests the need to evaluate the mediating effect of job-related stress in dealing with the subjective cognitive dysfunction associated with insomnia in workers.

List of Abbreviations

BJSQ

Brief Job Stress Questionnaire

COBRA

Cognitive Complaints in Bipolar Disorder Rating Assessment

FIRST-J

Japanese version of Ford Insomnia Response to Stress Test

n.s.

not significant

β

standardized regression coefficients

VIF

variance inflation factor

Declarations

Ethics approval and consent to participate

The present study was approved by the Local Ethics Committee of the Tokyo Medical University (Ethics Approval Number: SH3502). All participants provided written informed consent after receiving an explanation about the study.

Consent for publication

Not Applicable.

Availability of data and materials

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Competing interests

Jiro Masuya has received personal compensation from Otsuka Pharmaceutical, Eli Lilly, Astellas, and Meiji Yasuda Mental Health Foundation, as well as grants from Pfizer. Ichiro Kusumi has received honoraria from Daiichi Sankyo, Dainippon Sumitomo Pharma, Eisai, Eli Lilly, Janssen Pharmaceutical, Lundbeck, Meiji Seika Pharma, Mochida Pharmaceutical, MSD, Mylan, Novartis Pharma, Ono Pharmaceutical, Otsuka Pharmaceutical, Pfizer, Shionogi, Shire, Taisho Toyama Pharmaceutical, Takeda Pharmaceutical, Tsumura, and Yoshitomiyakuhin, and has received research/grant support from Asahi Kasei Pharma, Astellas, Daiichi Sankyo, Dainippon Sumitomo Pharma, Eisai, Eli Lilly, Mochida Pharmaceutical, Novartis Pharma, Otsuka Pharmaceutical, Pfizer, Shionogi, Takeda Pharmaceutical and Tanabe Mitsubishi Pharma. Takeshi Inoue is a member of the advisory boards of Pfizer, Novartis Pharma, and Mitsubishi Tanabe Pharma and has received personal fees from Mochida Pharmaceutical, Takeda Pharmaceutical, Eli Lilly, Janssen Pharmaceutical, MSD, Taisho Toyama Pharmaceutical, Yoshitomiyakuhin, and Daiichi Sankyo; grants from Shionogi, Astellas, Tsumura, and Eisai; and grants and personal fees from Otsuka Pharmaceutical, Dainippon Sumitomo Pharma, Mitsubishi Tanabe Pharma, Kyowa Pharmaceutical Industry, Pfizer, Novartis Pharma, and Meiji Seika Pharma. Yota Fujimura received research and grant support from Novartis Pharma, Otsuka Pharmaceutical, Astellas, Dainippon Sumitomo Pharma, and Shionogi. Shinji Higashi received honoraria from Dainippon Sumitomo Pharma and Novartis Pharma. Akiyoshi Shimura reports personal fees from Eisai, Sumitomo Dainippon Pharma, MSD, Yoshitomi Yakuhin Corporation, and Meiji Seika Pharma, outside the submitted work. Kuniyoshi Toyoshima does not have any actual or potential conflict of interest.

Funding

This work was partly supported by a Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Culture, Sports, Science and Technology [grant number 16K10194, to T. Inoue], Research and Development Grants for Comprehensive Research for Persons with Disabilities from the Japan Agency for Medical Research and Development [grant number JP18dk0307060, to T. Inoue], and SENSHIN Medical Research Foundation (to T. Inoue). The funding sources had no role in the study design; in the collection, analysis, and interpretation of data; in the writing of the report; or in the decision to submit the article for publication.

Authors’ contributions

All authors contributed toward data collection and reviewed and approved this manuscript.

KT: Writing - original draft, Data curation, Writing - review & editing. TI: Writing - original draft, Data curation, Writing - review & editing. AS: Data curation, Writing - review & editing. JM: Data curation, Writing - review & editing. YF: Data curation, Writing - review & editing. SH: Data curation, Writing - review & editing. IK: Data curation, Writing - review & editing.

Acknowledgments

The authors thank Dr. Nobutada Takahashi of Fuji Psychosomatic Rehabilitation Institute Hospital, Dr. Hiroshi Matsuda of Kashiwazaki Kosei Hospital, deceased Dr. Yasuhiko Takita of Maruyamasou Hospital, and Dr. Yoshihide Takaesu of Izumi Hospital for collecting data. The authors also thank their colleagues at Tokyo Medical University and Hokkaido University.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.


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