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. Author manuscript; available in PMC: 2023 Dec 1.
Published in final edited form as: J Affect Disord. 2022 Sep 1;318:94–102. doi: 10.1016/j.jad.2022.08.118

Delayed Circadian Rhythms and Insomnia Symptoms in Obsessive-Compulsive Disorder

Rebecca C Cox 1,2,*, Bunmi O Olatunji 1
PMCID: PMC10201922  NIHMSID: NIHMS1848128  PMID: 36057288

Abstract

Background:

Accumulating evidence implicates sleep and circadian rhythm disturbance in obsessive-compulsive disorder (OCD). However, a multimethod characterization of sleep and circadian rhythms in OCD, their association with symptom severity, and the functional relationship between these variables is lacking.

Methods:

The present study measured multiple indicators of sleep and circadian rhythms in a sample of adults with OCD, adults without OCD, and healthy controls (n=74). Participants completed measures of morningness-eveningness, delayed sleep-wake phase disorder (DSWPD), insomnia symptoms, and OCD symptoms, as well as one week of sleep monitoring via a sleep diary and actigraphy.

Results:

Delayed circadian rhythms (higher eveningness, later mid-sleep timing, and higher rates of DSWPD) and higher insomnia symptoms were observed in those with OCD compared to healthy controls, as well as associations between delayed circadian rhythms and insomnia symptoms and OCD symptom severity across the full sample. Further, insomnia symptoms mediated the relationship between delayed circadian rhythms and OCD symptoms. In contrast, there were no links between total sleep time or sleep quality and OCD.

Limitations:

Data collection during COVID-19 pandemic, correlational data, no physiological measure of circadian rhythms

Conclusions:

These findings highlight a robust association between delayed circadian rhythms and OCD and suggest insomnia symptoms may be one mechanism in this relationship. Sleep and circadian rhythm disturbance may be novel targets for OCD treatment.

Keywords: OCD, sleep, circadian rhythms, insomnia, eveningness, sleep timing

Obsessive-compulsive disorder (OCD) is a psychiatric condition characterized by intrusive, distressing thoughts (i.e., obsessions) and repetitive behaviors (i.e., compulsions) (American Psychiatric Association, 2013). Given the high degree of functional impairment experienced by those with OCD (Eisen et al., 2006), it is critical to identify modifiable mechanisms to inform etiological models and improve treatment outcomes. One such mechanism is sleep and circadian rhythm disturbance. Although sleep and circadian rhythm disturbance is broadly implicated in physical and mental health conditions (Harvey et al., 2011; Roenneberg and Merrow, 2016), its role in OCD has not been well characterized. Circadian rhythms are autonomous 24-hours cycles in processes ranging from gene expression to behavior that occur independent of environmental input (Roenneberg and Merrow, 2016). Stable and entrained circadian rhythms allow us to anticipate environmental demands and maintain synchrony between a host of processes in our bodies (Foster, 2020). Likewise, healthy sleep promotes neural (Xie et al., 2013), cognitive (Diekelmann, 2014; Diekelmann and Born, 2010), and emotional health (Tempesta et al., 2018).

Given the importance of sleep and circadian rhythms for a range of functions, it is perhaps unsurprising that sleep and circadian rhythm disturbance is associated with psychopathology, including OCD (Nota et al., 2015). Indeed, objective sleep studies have found evidence for decreased sleep duration in children and adults with OCD compared to healthy controls (Alfano and Kim, 2011; Insel et al., 1982; Rapoport et al., 1981; Voderholzer et al., 2007). Likewise, several studies have found associations between insomnia symptoms and OCD symptoms in community samples (Raines et al., 2015; Timpano et al., 2014), including prospective relations between insomnia symptoms and subsequent OCD symptoms (Cox et al., 2018c, 2018a), and high rates of subjective sleep disturbances are reported by patients with OCD (Storch et al., 2008). Although one recent study found high comorbidity between insomnia and OCD (Sevilla-Cermeño et al., 2020), few studies have compared subjective sleep disturbance in those with OCD to healthy controls, and extant findings have been mixed (Bobdey et al., 2002; Donse et al., 2017).

Accumulating evidence also links indicators of delayed circadian rhythms to OCD. For example, evening chronotype, or the tendency to prefer a later sleep/wake schedule and engage in activities (e.g., exercise, work, eating) later in the day (Horne and Ostberg, 1976), has been prospectively associated with increased OCD symptoms in a community sample (Cox et al., 2018c) and also predicts increased OCD symptoms in the morning among adults with OCD (Naftalovich et al., 2021). Further, adults with OCD exhibit a later dim light melatonin onset compared to healthy controls (Coles et al., 2020), which is one indicator of intrinsic circadian phase. Likewise, previous research has found a high rate of delayed sleep-wake phase disorder (DSWPD) in OCD (e.g., 40–42%) (Coles et al., 2020; Turner et al., 2007). Interestingly, extant research on sleep timing in OCD has been mixed. Though later bedtimes are associated with increased OCD symptom severity in adults with OCD (Nota et al., 2020; Schubert et al., 2019), one recent study found no difference in bedtimes between those with OCD compared to healthy controls (Coles et al., 2020). Further, no study to date has examined mid-sleep timing in OCD. Previous research indicates mid-sleep timing is highly correlated with physiological measures of circadian phase (Kantermann and Burgess, 2017) and more closely approximates circadian phase than bedtime (Reiter et al., 2020), suggesting the utility of examining this indicator of delayed circadian rhythms in OCD.

The extant literature points to sleep and circadian rhythm disturbance in OCD. Delayed circadian rhythms may contribute to sleep disturbance, particularly if these delays place the individual out of sync with environmental demands. Such desynchrony may contribute to insomnia symptoms and poor sleep quality due to trying to sleep at a time that is misaligned with circadian phase. Likewise, sleep duration may be curtailed if an individual initiates sleep late but must still wake up early to operate on typical schedules (e.g., school schedules, first shift). These sleep disturbances may then contribute to OCD, as sleep disturbance is implicated in numerous processes relevant to OCD, such as executive function (Drummond et al., 2006; Kuula et al., 2018) and emotion regulation (Palagini et al., 2017). Indeed, accumulating evidence suggests that sleep disturbances mediate the relationships between eveningness and mental health outcomes, including anxiety and depression symptoms (Dickinson et al., 2018; Zhou et al., 2021) and hospitalization for affective disorders (Merikanto and Partonen, 2021). However, no study to date has examined sleep disturbance as a mediator of the relationship between delayed circadian rhythms and OCD.

Although sleep and circadian rhythm disturbance has been implicated in OCD, no study to date has examined multiple indicators of sleep and delayed circadian rhythms in OCD, their association with symptom severity, and the functional relationship between these variables. The present study sought to address this gap in the literature using a multimethod approach. We hypothesized that those with OCD would exhibit delayed circadian rhythms, including higher eveningness, later mid-sleep timing, and higher rates of DSWPD, and more sleep disturbance, including higher insomnia symptoms, shorter objective and subjective sleep duration, and lower sleep quality, compared to healthy controls. We also hypothesized that indicators of delayed circadian rhythms and sleep disturbance would be associated with increased OCD symptoms and that sleep disturbance would mediate the relationship between delayed circadian rhythms and OCD symptoms in those with OCD, without OCD and healthy controls.

Methods

Participants

The sample consisted of undergraduate students and community adults with and without OCD (N = 80) who participated prior to and during the COVID-19 pandemic. Undergraduate students were recruited from psychology courses and were compensated with course credit. Community adults were recruited from flyers placed in the local community, including at OCD clinics, and a university research email notification system and were compensated with $50. Separate flyers with language recruiting adults with OCD or healthy adults were used. Participants who met criteria for moderate to high suicide risk (n = 2) or psychotic symptoms (n = 1) were withdrawn immediately and given appropriate referral information. An additional three participants withdrew prior to the second laboratory session due to scheduling issues or no longer being interested in participating. Seventy-four participants completed both study sessions.

The mean age of the sample was 23.99 years (SD = 7.21), ranging from 18 to 53 years (73% female). 59.7% were college-aged (18–22). The ethnicity composition was as follows: White (n = 42; 55%), Asian (n = 18; 23%), Black/African American (n = 9; 12%), Hispanic/Latino (n = 4; 5%), Other (n = 4; 5%). Twenty participants (27%) met criteria for OCD, and 29 participants (39%) were identified as healthy controls (i.e., met criteria for no disorders). An additional 25 (34%) participants who did not meet criteria for OCD but met criteria for another psychiatric disorder were included in the dimensional analyses. Sixty participants (75%) participated in data collection in person prior to the onset of the COVID-19 pandemic, and 20 participants (25%) participated in data collection virtually during the pandemic (see Procedure).

Measures

Diagnostic Status

The MINI International Neuropsychiatric Interview (MINI; Sheehan et al., 1998) is a well-validated and widely used semi-structured diagnostic interview that assesses for 17 DSM disorders. The MINI was used to determine diagnostic status.

Circadian rhythms

The Morningness-Eveningness Questionnaire (MEQ; Horne and Ostberg, 1976) is a 19-item self-report measure of morningness-eveningness preference (i.e., preferred time of day for activities such as sleep, eating, exercise, and work) and is thought to reflect, in part, the individual’s circadian rhythms. Items are rated on a Likert scale ranging from 1–6 with answer options varying by item content. Higher scores reflect morningness, and lower scores reflect eveningness. The MEQ demonstrated good internal consistency (α = 0.90) in the present study.

Mid-sleep is the midpoint between the time of sleep onset and sleep offset. Recent evidence suggests that a weekly average mid-sleep more closely approximates intrinsic circadian phase (Kantermann & Burgess, 2017) than mid-sleep on free days (Roenneberg et al., 2007); therefore, mean mid-sleep for the week (weekends included) was utilized. Variables for calculating mid-sleep were collected via the Consensus Sleep Diary (see below).

The Diagnostic Interview for Sleep Patterns and Disorders (DISPD; Merikangas et al., 2014) is a semi-structured diagnostic interview that assesses general sleep patterns and 8 DSM sleep disorders. Only the sleep patterns and delayed phase sleep syndrome modules were utilized in the present study to determine DSWPD diagnostic status.

Sleep disturbance

Actigraphy is an objective sleep measure that estimates sleep and wake from motion (Ancoli-Israel et al., 2003). The present study utilized ActiGraph wGT3X-BT activity monitors (ActiGraph, Pensacola, FL). Previous research indicates that actigraphy is highly accurate when compared to polysomnography (Marino et al., 2013) and that the ActiGraph wGT3X-BT is reliable and valid for estimating sleep (Cellini et al., 2013). Objective sleep duration was calculated with the Sadeh algorithm (Sadeh et al., 1994). Sleep periods were entered manually using participant-reported time into bed and time out of bed.

The Consensus Sleep Diary (CSD; Carney et al., 2012) is a 9-item sleep diary that asks participants about their last night of sleep, including subjective sleep duration. The CSD was developed by a panel of sleep experts to create a standard sleep diary for the assessment of daily sleep.

The Insomnia Severity Index (ISI; Bastien, Vallieres, & Morin, 2001) is a 7-item self-report measure of insomnia symptoms over the past two weeks and is used to detect cases of insomnia and assess treatment response. Items on the ISI are rated on a Likert scale from 0 (none) to 4 (very severe), and higher scores indicate higher insomnia symptom severity. The ISI demonstrated adequate internal consistency (α = 0.84) in the present study.

OCD symptoms

The Obsessive-Compulsive Inventory-Revised (OCIR; Foa et al., 2002) is an 18-item self-report measure of OCD symptoms in the past month. The OCIR consists of 6 subscales measuring specific categories of OCD symptoms (washing, checking, ordering, neutralizing, hoarding, obsessing). Items on the OCIR are rated on a Likert scale from 0 (not at all) to 4 (extremely), and higher scores indicated increased OCD symptom severity. The OCIR demonstrated adequate internal consistency (α = .88) in the present study.

Procedure

Data collection occurred over 9 consecutive days.

Prior to COVID-19 pandemic

On day 1, participants attended a laboratory session that included informed consent and administration of the MINI and DISPD. Following the interviews, participants completed the MEQ and ISI and then received an actigraph and CSD. On days 2 through 8, sleep was monitored continuously with actigraphy, and participants completed the CSD upon awakening each morning. On day 9, participants returned to the laboratory to complete the OCIR and be debriefed.

During COVID-19 pandemic

Following the onset of the COVID-19 pandemic, data collection was halted until June 25, 2020, on which date virtual data collection was initiated. Data was collected virtually on all self-report measures. Actigraphy data were not collected to avoid in-person encounters between researchers and participants. On day 1, participants attended a Zoom call that included informed consent and administration of the MINI and DISPD. The suicide module of the MINI was not completed virtually. Following the interviews, participants completed the MEQ and ISI and were given instructions for the week of daily sleep monitoring. On days 2 through 8, participants completed the CSD electronically upon awakening each morning. On day 9, participants attended a second Zoom call to complete the OCIR and be debriefed.

Data analysis

Between subjects t-tests were conducted to examine group differences in the MEQ, mid-sleep, ISI, subjective and objective sleep duration, and sleep quality between those with OCD and healthy controls. A chi square test was conducted to examine differences in rates of DSWPD between those with OCD and healthy controls. Associations between the MEQ, mid-sleep, DSWPD status, ISI, subjective and objective sleep duration, and sleep quality and OCIR were tested with separate linear regression models in the full sample, including those with OCD, those without OCD, and healthy controls. Each of these models controlled for participation before or during the COVID-19 pandemic (see Supplement for comparisons of study variables before and during COVID-19). Between subjects t-tests, the chi square test, and linear regressions were conducted in SPSS 27.

Two mediation models were tested examining the ISI as the mediator of the relationships between the MEQ status and DSWPD and the OCIR. A mediation model examining the ISI as the mediator of the relationship between mid-sleep and the OCIR was not tested, as mid-sleep was collected during the week of prospective sleep monitoring after collection of the ISI, which violates the assumption of temporal precedence of variables in a mediation model. The two mediation models were tested in Mplus 8 using full-information maximum likelihood estimation. Participation before or during the COVID-19 pandemic was included as a covariate. The significance of the indirect effects was tested by constructing a bias-corrected bootstrapped confidence interval around the indirect effects.

Results

Descriptive statistics and associations between study variables

Means, standard deviations, and bivariate correlations for study variables are shown in Table 1.

Table 1.

Descriptive statistics and correlations for study measures (n = 74).

Measure 1. 2. 3. 4. 5. 6. 7. 8. 9.
1. MEQ --
2. Mid-sleep −.70** --
3. DSWPD −.56** .39** --
4. ISI −.38** .25* .44** --
5. Obj sleep duration .16 −.34* −.07 −.06 --
6. Subj sleep duration .11 −.25* .02 −.21 .78** --
7. Sleep quality .13 −.03 −.17 −.34** .11 .17 --
8. OCIR −.36* .30* .33* .36* .16 .02 .01 --
9. COVID .22 −.26* −.08 −.03 N/A .28* −.04 −.18 --
M 48.05 4.50 8.44 388.30 418.30 3.35 16.59
SD 12.18 1.35 5.01 61.41 64.27 .68 11.31
Range 22–75 1.70–7.55 1–18 210.60–516.00 213.00–575.00 2–5 0–51
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Note. MEQ=Morningness-Eveningness Questionnaire; Mid-sleep=mid-sleep timing (decimal format); DSWPD=delayed sleep-wake phase disorder status; ISI=Insomnia Severity Index; Obj = objective; Subj = subjective; OCIR=Obsessive-Compulsive Inventory-Revised; COVID=participation before/during COVID-19.

*

p < .05

**

p < .01

Group differences in circadian rhythms

Results of between subjects t-tests and a chi square analysis indicated delayed circadian rhythms in those with OCD compared to healthy controls (see Figure 1). Specifically, those with OCD reported significantly lower morningness (i.e., higher eveningness) (M = 40.60, SD = 9.54) compared to healthy controls (M = 53.66, SD = 13.15), t(47) = −3.80, p < .001, d = −1.10, 95% CI [−1.71, −.49], and significantly later mid-sleep timing (M = 4.93, SD = 1.21) compared to healthy controls (M = 4.02, SD = 1.33), t(45) = 2.41, p < .05, d = .71, 95% CI [.11, 1.30]. There was also a significant relationship between OCD and DSWPD status, χ2(2, n=49) = 13.86, p < .001, ϕ = .53, 95% CI [.34, .71], such that 40% of those with OCD also met criteria for DSWPD, compared to 0% of healthy controls (see Figure 2).

Figure 1.

Figure 1.

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Mean differences in mid-sleep timing and the Morningness-Eveningness Questionnaire between those with OCD and healthy controls. Error bars represent +/− one standard error.

Figure 2.

Figure 2.

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Distribution of comorbid DSWPD diagnosis in those with OCD compared to healthy controls.

Associations between circadian rhythms and OCD symptoms

Results of multiple linear regression models found that delayed circadian rhythms significantly predicted higher OCD symptoms across the full sample (see Table 2). The model with morningness-eveningness as the predictor was significant, R2 = .37, F (2,71) = 5.72, p < .01, and lower morningness (i.e., higher eveningness) significantly predicted higher OCD symptoms, β = −.33, p < .01, controlling for participation before or during the COVID-19 pandemic, β = −.11, p = .35. Similarly, the model with mid-sleep timing as the predictor was significant, R2 = .11, F (2,69) = 4.04, p < .05, and later mid-sleep timing significantly predicted higher OCD symptoms, β = .27, p < .05, controlling for participation before or during the COVID-19 pandemic, β = −.13, p = .28. Finally, the model with DSWPD status as the predictor was significant, R2 = .13, F (2,72) = 5.41, p < .01, and DSWPD significantly predicted higher OCD symptoms, β = .31, p < .01, controlling for participation before or during the COVID-19 pandemic, β = −.16, p = .14.

Table 2.

Model coefficients for the hypothesized regression models predicting OCD symptoms from morningness-eveningness (Model 1), mid-sleep timing (Model 2), and DSWPD status (Model 3), controlling for participation before/during COVID-19 (n = 74).

Model 1
Predictor B SE β t p
Step 1
COVID −4.65 2.93 −.18 −1.59 .12
Step 2
COVID −2.70 2.87 −.11 −.94 .35
MEQ −.31 .10 −.33 −2.94 <.01
Model 2
Predictor B SE β t p
Step 1
COVID −5.01 2.96 −.20 −1.70 .10
Step 2
COVID −3.27 2.98 −.13 −1.10 .28
Mid-sleep 2.23 .99 .27 2.25 <.05
Model 3
Predictor B SE β t p
Step 1
COVID −4.88 2.94 −.19 −1.66 .10
Step 2
COVID −4.19 2.82 −.17 −1.49 .14
DSWPD 9.81 3.51 .31 2.79 <.01
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Note. MEQ=Morningness-Eveningness Questionnaire; Mid-sleep=mid-sleep timing (decimal format); DSWPD=delayed sleep-wake phase disorder status; COVID=participation before/during COVID-19.

Group differences in sleep disturbance

Results of between subject t-tests largely did not indicate more sleep disturbance in those with OCD compared to healthy controls. Specifically, those with OCD did not exhibit significantly different subjective sleep duration (M = 413.49, SD = 66.05) compared to healthy controls (M = 438.41, SD = 51.04), t(45) = −1.46, p = .15, d = −.43, 95% CI [−1.0, .16], or objective sleep duration (M = 387.43, SD = 77.06) compared to healthy controls (M = 403.12, SD = 55.42), t(27) = −.63, p = .53, d = −.24, 95% CI [−.96, .50]. Likewise, those with OCD did not exhibit significantly different subjective sleep quality (M = 3.28, SD = .58) compared to healthy controls (M = 3.45, SD = .66, t(45) = −.93, p = .36, d = −.27, 95% CI [−.85, .31]. However, those with OCD did report significantly higher insomnia symptoms (M = 11.10, SD = 5.03) compared to healthy controls (M = 5.90, SD = 4.22), t(47) = 3.92, p < .001, d = 1.14, 95% CI [.52, 1.75] (see Figure 3).

Figure 3.

Figure 3.

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Mean difference in the Insomnia Severity Index between those with OCD and healthy controls. Error bars represent +/− one standard error.

Associations between sleep disturbance and OCD symptoms

Results of multiple linear regression models found that sleep disturbance was largely unrelated to OCD symptoms across the full sample, with the exception of insomnia symptoms (see Table 4). The model with insomnia symptoms as the predictor was significant, R2 = .16, F (2,71) = 6.66, p < .01, and higher insomnia symptoms significantly predicted higher OCD symptoms, β = .35, p < .01, controlling for participation before or during the COVID-19 pandemic, β = −.17, p = .13. In contrast, models predicting OCD symptoms from subjective sleep duration, objective sleep duration, and sleep quality were not statistically significant, p’s > .05.

Table 4.

Unstandardized model coefficients for mediation model 1 with MEQ as the indicator of eveningness (n = 77) and mediation model 2 with DSWPD status as the indicator of eveningness (n = 76), controlling for participation before/during COVID-19.

Model 1
ISI (M) OCIR (Y)
Predictor B SE p B SE p
MEQ (X) −.16 .05 <.001 −.21 .10 <.05
ISI (M) .60 .26 <.05
COVID (covariate) .65 1.34 .63 −3.03 2.81 .28
R2 = .15, p = .06 R2 = .20, p < .01
Model 2
ISI (M) OCIR (Y)
B SE p B SE p
DSWPD (X) 6.23 1.35 <.001 5.97 23.87 .12
ISI (M) .62 .23 <.05
COVID (covariate) .10 1.30 .94 −4.19 2.80 .13
R2 = .19, p < .05 R2 = .19, p <.05
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Note. MEQ = Morningness-Eveningness Questionnaire; ISI = Insomnia Severity Index; OCIR = Obsessive-Compulsive Inventory-Revised; COVID = participation before/during COVID-19; DSWPD = Delayed sleep-wake phase disorder diagnosis.

Mediation models

All regression coefficients in mediation models are reported as unstandardized values. Results of model 1 utilizing the MEQ as the indicator of circadian rhythms found that morningness-eveningness significantly predicted OCD symptoms through its effects on insomnia symptoms, controlling for participation before or during the COVID-19 pandemic. Lower morningness (i.e., higher eveningness) significantly predicted higher insomnia symptoms (a = −.21, p < .05), which in turn significantly predicted higher OCD symptoms (b = .60, p < .05). A 95% confidence interval around the indirect effect (ab = −.10) based on 10,000 bootstrap samples did not contain zero (−.24 to −.02), indicating a significant mediating effect of insomnia symptoms in the relationship between morningness-eveningness and OCD symptoms (see Table 4, Figure 4).

Figure 4.

Figure 4.

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Unstandardized path coefficients for the hypothesized mediation model, in which insomnia symptoms significantly mediate the relationship between delayed circadian rhythms (indicated by the Morningness-Eveningness Questionnaire) and OCD symptoms, controlling for participation before/during COVID-19 (n = 77). * p < .05.

Results of model 2 utilizing DSWPD status as the indicator of circadian rhythms likewise found that DSWPD significantly predicted OCD symptoms through its effects on insomnia symptoms, controlling for participation before or during the COVID-19 pandemic. DSWPD significantly predicted higher insomnia symptoms (a = 6.23, p < .001), which in turn significantly predicted higher OCD symptoms (b = .62, p < .05). A 95% confidence interval around the indirect effect (ab = 3.89) based on 10,000 bootstrap samples did not contain zero (.99 to 8.53), indicating a significant mediating effect of insomnia symptoms in the relationship between DSWPD status and OCD symptoms (see Table 4, Figure 5).

Figure 5.

Figure 5.

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Unstandardized path coefficients for the hypothesized mediation model, in which insomnia symptoms significantly mediate the relationship between delayed circadian rhythms (indicated by the delayed sleep-wake phase disorder [DSWPD] diagnosis) and OCD symptoms, controlling for participation before/during COVID-19 (n = 76). * p < .05.

Discussion

The present study examined sleep and circadian rhythm disturbance in OCD and relationships between delayed circadian rhythms, sleep disturbance, and OCD symptom severity. Results indicated delayed circadian rhythms in adults with OCD compared to healthy controls, such that large effects for delayed circadian rhythms in OCD were observed across multiple measures, including morningness-eveningness, mid-sleep timing, and DSWPD status. These findings are consistent with previous research linking indicators of delayed circadian rhythms to OCD symptoms, including eveningness (Cox et al., 2018c), dim light melatonin onset, and DSWPD status (Coles et al., 2020). Though previous work has linked later bedtimes to OCD symptoms (Nota et al., 2020), this is the first study to find later mid-sleep timing in those with OCD compared to controls. Mid-sleep is a better indicator of sleep timing, as it reflects the timing of the total sleep period, and is more strongly associated with intrinsic circadian phase than bedtime (Reiter et al., 2020). Further, the large effect sizes found across multiple indicators of circadian rhythms suggest a robust effect for delayed circadian rhythms in OCD compared to healthy controls.

The present finding that 40% of those with OCD also met criteria for DSWPD replicates previous studies finding an almost identical rate of DSWPD in OCD (i.e., 40–42%) (Coles et al., 2020; Turner et al., 2007). Further, across the full sample, delayed circadian rhythms were associated with increased OCD symptom severity, suggesting circadian rhythm disturbance may also underpin subthreshold OCD symptoms. Though research in this area is nascent, several potential mechanisms may account for the link between delayed circadian rhythms and psychiatric outcomes, including interactions between the circadian and reward systems, social jetlag (Alloy et al., 2015; Taylor and Hasler, 2018), impaired executive function (Wulff et al., 2010), and neural systems involved in mood regulation (McClung, 2013). Additional research is needed to clarify the mechanism(s) linking delayed circadian rhythms to OCD specifically.

In contrast, evidence for sleep disturbance in OCD was mixed. There was a large, significant difference found for insomnia symptoms, such that those with OCD reported higher insomnia symptoms compared to healthy controls. This study is the first to compare insomnia symptom severity between those with OCD and healthy controls, though previous research has found significant associations between insomnia symptoms and OCD symptoms in clinical (Sevilla-Cermeño et al., 2020, 2019) and nonclinical samples (Raines et al., 2015; Timpano et al., 2014). This suggests that the link between insomnia and OCD is robust and independent of categorical versus dimensional conceptualizations of the disorder. Although the present study also found that higher insomnia symptoms were significantly associated with higher OCD symptoms across the full sample, no significant differences were found between those with OCD and healthy controls on objective or subjective sleep duration. Notably, insomnia is a disorder of sleep continuity and is not necessarily characterized by short sleep duration (Means et al., 2003). Likewise, the existing literature utilizing prospective sleep monitoring in OCD is mixed. Though some studies have found decreased sleep duration in OCD compared to healthy controls (Alfano and Kim, 2011; Donse et al., 2017), other studies have found no such differences (Coles et al., 2020; Jaspers-Fayer et al., 2018). However, one study did find evidence for decreased sleep quality in pediatric OCD (Jaspers-Fayer et al., 2018), in contrast with the present findings. Still, studies utilizing polysomnography have found a consistent effect for decreased sleep duration in OCD (Insel et al., 1982; Rapoport et al., 1981; Voderholzer et al., 2007); thus, multiple objective and subjective measures of sleep are needed in future research to characterize sleep disturbance in OCD.

The present study also examined the extent to which insomnia symptoms mediated the relationship between delayed circadian rhythms and OCD using morningness-eveningness and DSWPD status as the indicators of circadian rhythms, controlling for participation before or during the COVID-19 pandemic. Both eveningness and DSWPD significantly predicted higher insomnia symptoms. Eveningness and DSWPD have consistently been associated with sleep disturbance, including insomnia symptoms (Merikanto et al., 2012; Sivertsen et al., 2013) and increased variability in sleep (Bei et al., 2016; Burgess et al., 2017). Delayed circadian rhythms may interfere with sleep through several mechanisms. Insomnia symptoms may develop among those with delayed circadian timing who are attempting to initiate sleep at an earlier time that is inconsistent with their internal circadian phase. Those with delayed circadian rhythms may also attempt to fit their sleep timing to environmental demands during the week (e.g., the need be at work by 8:00am), and then sleep on a schedule that is more consistent with their internal circadian phase on the weekends. Such variability in sleep timing may then contribute to insomnia symptoms by interfering with consistent circadian entrainment (e.g., morning light exposure is received at variable times) and/or contributing to variability in homeostatic sleep pressure on subsequent nights.

Insomnia symptoms also significantly predicted higher OCD symptoms in the mediation model, which is consistent with previous research implicating sleep disturbance in OCD (Cox et al., 2018b; Nota et al., 2015). In both mediation models, the effects of eveningness and DSWPD on increased OCD symptoms were significantly mediated by insomnia symptoms. Though previous research has linked DSWPD to psychopathology broadly (Reid et al., 2012) and OCD specifically (Coles et al., 2020), this study offers the first evidence for the mediating role of insomnia in this relationship. These models suggest that delayed circadian rhythms may contribute to increased OCD symptoms through an effect on sleep. For example, those with delayed circadian timing may experience insomnia symptoms or poor sleep quality when attempting to sleep on a schedule that is misaligned with their circadian phase. These sleep disturbances may then confer vulnerability for increased OCD symptoms. This interpretation is supported by prior research showing that sleep disturbance mediates the effect of eveningness on mental health outcomes, including depression and anxiety symptoms (Dickinson et al., 2018; Merikanto and Partonen, 2021; Zhou et al., 2021). The present findings also complement previous research showing a mediating effect of insomnia symptoms between eveningness and OCD symptoms over 6 months in a sample of unselected adults (Cox et al., 2018c).

The present study found robust evidence for delayed circadian rhythms and insomnia symptoms in OCD. There was also evidence for associations between delayed circadian rhythms and insomnia symptoms and OCD symptoms across the full sample, as well as evidence for a mediating role of insomnia symptoms in the relationship between delayed circadian rhythms and OCD symptoms. These findings may have important implications for the assessment and treatment of OCD. For example, consideration should be given to the routine assessment of sleep and circadian rhythms in OCD patients. Indeed, the finding that 40% of the OCD group met criteria for DSWPD suggests that DSWPD is an important yet overlooked OCD comorbidity. Further, a recent study found that later sleep timing predicted treatment non-response in those with OCD treated with exposure and response prevention (Coles et al., 2021). Thus, targeting sleep and circadian rhythms through evidence-based therapies such as social rhythm therapy, CBTI, or bright light therapy may improve OCD treatment efficacy. Indeed, inpatient OCD treatment facilities with a set “lights out” time have a higher rate of treatment response (Coles and Stewart, 2019), suggesting that consistent timing of circadian entrainment cues may be therapeutic for OCD. Likewise, circadian-based treatments have shown promise for improving mental health outcomes in evening chronotypes (Dong et al., 2019; Facer-Childs et al., 2019). Although no study to date has examined the impact of sleep interventions on OCD symptoms, previous meta-analyses indicate that CBTI is associated reduced general anxiety (Belleville et al., 2011) and PTSD symptoms (Ho et al., 2016), suggesting that targeting insomnia symptoms in OCD treatment may have similar effects.

The present study found evidence for roles of delayed circadian rhythms and insomnia symptoms in OCD. However, these findings should be considered within the context of the study limitations. First and most notably, the onset of the COVID-19 pandemic resulted in approximately 1/3 of the sample participating virtually and limited actigraphy data collection. Although dimensional analyses included time of participation as a covariate, it is possible that the unprecedented nature of a global pandemic impacted these results over and above what could be accounted for by this covariate. Second, though multiple indicators of circadian rhythms were utilized, we did not include an objective measure of circadian phase, such as dim light melatonin onset, which may better capture intrinsic circadian rhythms. Third, the lack of an experimental manipulation and the cross-sectional nature of the data precludes the ability to make a causal inference regarding the direction of the relationships between delayed circadian rhythms, insomnia symptoms, and OCD (Cole and Maxwell, 2003); thus, the pathways proposed here will need to be tested using experimental and longitudinal designs. Fourth, given the relative homogeneity of the sample demographics (e.g., majority female, majority younger adults), it will be important to replicate these findings in diverse samples. Fifth, we were underpowered to examine the specificity of the observed effects in OCD compared to those with other psychiatric disorders; however, this is an important area for future research. Despite these limitations, this study offers additional support for delayed circadian rhythms and insomnia symptoms in those with OCD and provides the first evidence for a mediating role of insomnia symptoms in the relationship between delayed circadian rhythms and OCD symptom severity. Future research is needed to further delineate the mechanisms linking sleep and circadian rhythm disturbance to OCD and explore their potential for improving OCD treatment outcomes.

Supplementary Material

1

Table 3.

Model coefficients for the hypothesized regression models predicting OCD symptoms from insomnia symptoms (Model 1), subjective total sleep time (Model 2), and sleep quality (Model 4), controlling for participation before/during COVID-19 (n = 74). Model 3 predicting OCD symptoms from objective total sleep time does not control for time of participation, as actigraphy data was only collected prior to the COVID-19 pandemic.

Model 1
Predictor B SE β t p
Step 1
COVID −4.65 2.93 −.18 −1.59 .12
Step 2
COVID −4.28 2.76 −.17 −1.55 .13
ISI .79 .24 .35 3.24 <.01
Model 2
Predictor B SE β t p
Step 1
COVID −4.65 2.93 −.18 −1.59 .12
Step 2
COVID −5.68 3.07 −.22 −1.85 .07
Subj TST .03 .02 .14 1.12 .27
Model 3
Predictor B SE β t p
Step 1
Obj TST .03 .03 .16 1.10 .27
Model 4
Predictor B SE β t p
Step 1
COVID −4.88 2.94 −.19 −1.66 .10
Step 2
COVID −4.79 2.96 −.19 −1.62 .11
Sleep quality .05 .13 .05 .38 .70
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Note. ISI=Insomnia Severity Index; Subj TST=subjective total sleep time; Obj TST=objective total sleep time; COVID=participation before/during COVID-19.

Highlights.

  • The OCD group exhibited delayed circadian rhythms and higher insomnia symptoms

  • Delayed circadian rhythms were associated with OCD symptom severity

  • Insomnia symptoms mediated this effect

Acknowledgments.

The authors would like to acknowledge Allison Booher, Yunfeng Deng, Sarah Jessup, Max Luber, Angelee Parmar, Maria Sanin, and Yunshu Yang for their assistance with data collection.

Funding.

This work was supported by the National Institute of Mental Health of the National Institutes of Health [F31MH113271] and the National Heart, Lung, and Blood Institute (T32HL149646). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

Footnotes

CRediT authorship contribution statement. Rebecca C. Cox: Conceptualization, Methodology, Software, Formal analysis, Investigation, Writing-Original draft, Visualization, Funding acquisition. Bunmi O. Olatunji: Conceptualization, Methodology, Resources, Writing-Review and editing, Supervision.

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Declaration of Interest. None

Declaration of interests

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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