Association of job stress, CLOCK gene polymorphism and their interaction with poor sleep quality

Abstract

Job stress and the Circadian Locomotor Output Cycles Kaput (CLOCK) gene could affect circadian rhythm and sleep quality. The main aim of our present study was to investigate the association of job stress, CLOCK gene polymorphism and their interaction with sleep quality in a non‐clinical Chinese Han population, which has not been reported to date. Using a cross‐sectional design, 450 subjects were recruited in Beijing. Sleep quality was measured with the Pittsburgh Sleep Quality Index (PSQI) and job stress was measured with the Work Stress Scale. CLOCK gene rs11932595 polymorphism was genotyped in 297 blood samples. Correlation analysis showed a close but different association of high job stress with the PSQI and its components. Analysis of variance showed significant main effects of the CLOCK gene rs11932595 polymorphism. G‐allele carriers had a higher score in the PSQI, sleep duration, sleep latency and sleep disturbances. Further interaction analyses showed an ordinal interaction on sleep duration, and a disordinal interaction on daytime dysfunction. Specifically, G‐allele carriers had poorer sleep duration than AA homozygotes when in high job stress, while the two subgroups displayed similar sleep duration when in low job stress, conforming to the diathesis–stress model. In comparison to G‐allele carriers, AA homozygotes experienced less daytime dysfunction when in low job stress whereas more daytime dysfunction when in high job stress, fitting with the differential susceptibility model. As genetic links have been revealed, our investigation might be conducive for elucidating aetiological factors for sleep quality and targets for implementing interventions to attain good sleep quality.

Association of occupational stress, period circadian regulator 3 (PER3) gene polymorphism and their interaction with poor sleep quality

“…These findings indicated that employees with high or medium occupational stress are at higher risk of poor sleep quality than those with low occupational stress. A cross‐sectional study of 450 subjects conducted by Li et al also support this view, and their correlation analysis revealed a close but different relationship between high job stress and the components of the PSQI (Li et al., 2020). Alterations in neurobiological characteristics (i.e.…”

“…However, no evidence was found for an association between PER3 VNTR gene polymorphism and both sleep quality and diurnal preference in a twin longitudinal study (Barclay et al, 2011). (Antypa et al, 2012;Huang et al, 2014;Jiang et al, 2016;Li et al, 2015Li et al, , 2020…”

“…In addition, other studies have acknowledged that these factors work in concert to influence sleep via processes such as a gene–occupational stress interaction. Recent literature indicates the interactions between serotonin transporter‐gene‐linked polymorphic region ( 5‐HTTLPR ), 5‐hydroxytryptamine receptor type 2A ( 5‐HTR2A ), clock circadian regulator ( CLOCK ) and PER2 gene polymorphisms and occupational stress on sleep disorders (Antypa et al., 2012; Huang et al., 2014; Jiang et al., 2016; Li et al., 2015, 2020). Yet research assessing the interplay between PER3 VNTR gene polymorphism and occupational stress influences focussed on sleep quality is scarce.…”

Every Night and Every Morn: Effect of Variation in CLOCK Gene on Depression Depends on Exposure to Early and Recent Stress

“…In another study in bipolar disorder patients, a significant interaction between CLOCK variants and early stress exposure on hopelessness and suicide in BP patients was reported (47). In a non-clinical Chinese population, G allele of rs11932595 was associated with altered sleep duration only in those exposed to high job stress, but showed no effect in case of low stress, while AA carriers showed less daytime dysfunction under low stress and more in high stress conditions compared to G carriers suggesting not only a geneenvironment interaction effect, but also the role of the CLOCK as both a vulnerability and resilience gene with both positive and negative effects depending on stress (68).…”

“…For example, fluoxetine normalizes disrupted lightinduced entrainment, fragmented ultradian rhythms and altered hippocampal CLOCK expression in animal models of depression (107), while agomelatine, a melatonergic antidepressant is hypothesized to resynchronize disrupted circadian rhythms (108, 109). It has also been suggested that CLOCK expression may predict efficacy of antidepressants exerting their effects via influencing circadian mechanisms (68). Thus, understanding the role of CLOCK variation in depression may help identify new targets for pharmacological treatment possibly via modulating the impact of stress on brain function (7) as well as prediction of efficacy especially in subtypes of depression aiding precision therapy.…”