Objectives: This meta-analysis aimed to examine the association between chronotype and insomnia.

Methods: A systematic search of PubMed, Embase, and the Cochrane Library was conducted to identify prospective and cross-sectional studies published before July 2023. Sixteen studies involving 27,789 participants were included. Chronotype was assessed using the Morningness-Eveningness Questionnaire. Odds ratios with 95% confidence intervals were calculated for dichotomous outcomes, and mean differences with 95% confidence intervals were used for continuous outcomes. Random-effects models were applied in the presence of moderate-to-high heterogeneity. Sensitivity and subgroup analyses were performed to assess robustness and consistency.

Results: Compared with morning types, evening chronotypes had a significantly higher risk of insomnia (odds ratio, 3.47; 95% confidence interval, 2.50-4.83; P<.00001) and higher ISI scores (mean difference, 3.00; 95% confidence interval, 1.70-4.30; P<.00001). Intermediate chronotypes also showed elevated risk (odds ratio, 1.61; 95% confidence interval, 1.24-2.09; P = .0004) and moderately higher ISI scores (mean difference, 1.55; 95% confidence interval, 0.47-2.63; P = .005) compared with morning types.

Conclusion: Individuals with an evening chronotype were more likely to report insomnia symptoms compared with those with morning or intermediate chronotypes. Intermediate chronotypes tended to have a moderate association, while morning types showed the lowest likelihood of reporting insomnia symptoms. These findings highlight the importance of considering chronotype in the assessment and management of insomnia.

Increased waste clearance in the brain is thought to occur most readily during deep sleep (stage N3). Sleep deprivation disrupts time spent in deeper sleep stages, fragmenting the clearance process. Here, we have utilized the publicly available Stockholm Sleepy Brain Study to investigate whether various sleep-related measures are associated with changes in perivascular space (PVS) volume fraction following a late-night short-sleep experiment. The study sample consisted of 60 participants divided into old (65–75 years) and young (20–30 years) age groups. We found that partial sleep deprivation was not significantly associated with major PVS changes. In our centrum semiovale models, we observed an interaction between percentage of total sleep time spent in N3 and sleep deprivation status on PVS volume fraction. In our basal ganglia models, we saw an interaction between N2 (both percentage of total sleep time and absolute time in minutes) and sleep deprivation status. However, the significance of these findings did not survive multiple comparisons corrections. This work highlights the need for future longitudinal studies of PVS and sleep, allowing for quantification of within-subject morphological changes occurring in PVS due to patterns of poor sleep. Our findings here provide insight on the impact that a single night of late-night short-sleep has on the perivascular waste clearance system.

Study Objectives: Insomnia disorder, affecting 10% of the population, poses a significant public health concern and is a risk-factor for many health issues. Cognitive behavioral therapy is first-choice treatment, but the key component—sleep restriction therapy—presents with side effects and adherence challenges. Sleep compression therapy, suggested as a potentially gentler alternative, has never been directly compared to sleep restriction therapy. Methods: Single-blind trial at the Internet Psychiatry Clinic in Stockholm, Sweden. Patients with insomnia disorder were randomized 1:1 to evaluate non-inferiority of sleep compression therapy to sleep restriction therapy in improving insomnia and to compare important clinical aspects. Primary outcome: self-reported Insomnia Severity Index (ISI), assessed pretreatment, weeks 1–5, and week 10. Non-inferiority analysis based on intent-to-treat analyses with multiple imputation and mixed effects models. Results: Adults with insomnia (n = 234; mean age 44.3 [SD = 13.7] years, 173 [73.4%] female) received treatment as a 10-week highly structured, therapist-guided online program, to strengthen experimental integrity and treatment fidelity. Both treatments improved insomnia severity with large effects. Sleep compression therapy failed to show non-inferiority with a conservative limit of 1.6 ISI-points (95% CI: −0.01, 1.70), gave statistically significantly smaller improvements (p = .006), and was associated with slower improvements despite better adherence and somewhat less side effects. Conclusions: This direct comparison and well-controlled trial provides empirically based support for clinicians to prioritize sleep restriction therapy over sleep compression therapy, while the latter can be a valid alternative when sleep restriction therapy cannot be used.

While sleep characteristics have been associated with cardiovascular disease (CVD), most studies have focused on single timepoints or isolated aspects. The prognostic value of broader, long-term sleep patterns remains unclear.

We used data from 24,223 participants in the Swedish Longitudinal Occupational Survey of Health (SLOSH), with biennial follow-up between 2010 and 2018. Sleep characteristics were assessed via self-report and incident cardiovascular outcomes were identified through linkage to national registers. Cox proportional hazards models estimated associations between sleep variables and incident cardiovascular disease, and mixed-effects models assessed sleep trajectories.

During follow-up, 1,687 developed cardiovascular outcomes. Nighttime insomnia was not associated with increased CVD risk unless accompanied by daytime symptoms (HR 1.22, 95 % CI 1.03–1.44; reference: no insomnia and no daytime symptoms). Similarly, long sleep duration (>8 h) was associated with higher risk only when combined with daytime symptoms (HR 1.35, 95 % CI 1.13–1.61; reference: 6–8 h of sleep and no daytime symptoms). Trajectory analyses showed that participants with long sleep at baseline who later developed CVD had a gradual increase in sleep duration over time (β for CVD >8 h × time = 0.06, 95 % CI 0.04–0.07; β × time² = −0.005, 95 % CI –0.01 to 0.00), while long sleepers who remained free of CVD showed stable or declining patterns.

Daytime symptoms, particularly when accompanied by prolonged or increasing sleep, may reflect early physiological changes preceding cardiovascular disease. These findings highlight the importance of considering sleep patterns and changes over time rather than static measures alone.

Cognitive behavioural therapy for insomnia includes methods to adjust bedtimes and risetimes. The most well-known is sleep restriction therapy, but alternatives like sleep compression therapy and bedtime regularization also exist. Instructions and terminology vary. This scoping review uses “time-in-bed manipulation therapy” to encompass all such interventions, aiming to synthesize information on their implementation in adult populations, focusing on different instructions found in the literature. We searched five electronic databases. Two independent reviewers screened full-text papers, followed by data extraction. Both quantitative (e.g., instruction frequencies) and qualitative (e.g., analysis of content) syntheses were conducted. Of 7474 citations and 500 full-text papers, 52 studies met inclusion criteria, covering 60 therapies. Most interventions were termed sleep restriction therapy, but other names, such as sleep compression and bedtime restriction, were also used. Nine different methods for calculating the initial sleep window were identified, with further variation in other instructions. About half of the studies were randomized controlled trials. This review provides a comprehensive overview of time-in-bed manipulation therapies, aiding researchers and clinicians in selecting appropriate approaches. It highlights the need for clearer reporting, increased direct comparisons, and suggests a new model, The Restriction and Flexibility Model, describing key dimensions of these interventions.

This is a personal review of a research life focused on sleep in everyday life. It finds that irregular work hours shorten sleep duration and increase sleepiness, both subjectively and objectively (polysomnography). Also, experimental lab studies demonstrate reduced sleep duration (and sleep stages N2 and REM) when sleep is moved into the daylight hours (and the circadian upswing). Stage N3% seems not affected, and homeostatic experiments suggest that awakenings should not occur until the need for N3% or total spectral power has been satisfied. Furthermore, sleepiness is associated with increased alpha activity and slow eye movements, although the best indicator of dangerous sleepiness is subjective ratings (linked to perceptions of heavy eye lids). Everyday stress has very modest negative effects on objective sleep quality. Sleep loss as well as excessive sleep durations are linked to mortality, but with modest risk, and mainly in older individuals. Finally, objective sleep poorly reflects subjective sleep quality, and women appear to report poorer sleep than men, while objective data show better sleep quality in women. The discrepancy is considerably greater in older age groups.

Background: Sickness absence has been linked to short and long, as well as poor, sleep in a few studies. Such studies have started from a baseline measurement and followed up on subsequent sickness absence. In the present study, however, we focused on the change in biennial reports of sickness absence and sleep measures (using work-related variables as possible modifiers). We also searched for an interaction between predictors and gender since women report more sleep problems. Methods: A total of 5377 individuals (random sample from the Swedish working population) participated across five biennial points of measurement. Data were analyzed using mixed-model logistic regression. Results: The multivariable analysis of variation across the five time points showed that the significant sleep-related predictors of sickness absence (at least one occurrence during the preceding year) were sleep duration during days off (OR = 1.16, 95% Cl = 1.08;1.24) and sleep problems (OR = 1.42, 95% CI = 1.33;1.51). These also remained significant after the addition of psychosocial work factors. Sensitivity analyses indicated that a 9 h sleep duration during days off may represent a critical level in terms of increased sickness absence and that late rising contributed to the association between sickness absence and long sleep duration during days off. Women reported a higher sickness absence than men (OR = 2.16, 95% CI = 1.74;2.68) and had a higher probability of sickness absence for long sleep during days off and during the workweek than men. Conclusions: It was concluded that increases in sleep problems and sleep duration during days off are longitudinally associated with changes in sickness absence and that women have a closer link between the two. This suggests that treatment for sleep problems may reduce the risk of sickness absence.

The nature of the relationship between sleep problems and dementia remains unclear. This study investigated the relationship between sleep measures and dementia in older adults (≥ 65) using data from the English Longitudinal Study of Ageing (ELSA) and further investigated the causal association in Mendelian randomization (MR) analysis. In total of 7,223 individuals, 5.7 % developed dementia (1.7 % Alzheimer's disease (AD)) within an average of 8 (± 2.9) years. Cox regression models and MR were employed. Long sleep duration (>8 h) was associated with 64 % increased risk of incident dementia and 2-fold high risk of AD compared to ideal sleep duration (7–8 h). This association was particularly evident in older-older adults (≥70 years) and those who consumed alcohol. Short sleep duration (<7 h) was associated with lower risk of incident dementia among older-older but higher risk among younger-older adults. Sleep disturbances and perceived sleep quality were not associated with dementia or AD. The MR study did not reveal causal associations between sleep duration and dementia. These findings suggest that self-reported short sleep in younger-older and long sleep in older-older adults and those with frequent alcohol consumption are associated with dementia. Early detection of these sleep patterns may help identify individuals at higher dementia risk.

Both short (< 6 hr) and long (> 8 hr) sleep are associated with increased mortality. We here investigated whether the association between sleep duration and all-cause, cardiovascular disease and cancer mortality differs between men and women. A cohort of 34,311 participants (mean age and standard deviation = 50.5 ± 15.5 years, 65% women), with detailed assessment of sleep at baseline and up to 20.5 years of follow-up (18 years for cause-specific mortality), was analysed using Cox proportional hazards model to estimate HRs with 95% confidence intervals. After adjustment for covariates, all-cause, cardiovascular disease and cancer mortalities were increased for both < 5 hr and ≥ 9 hr sleep durations (with 6 hr as reference). For all-cause mortality, women who slept < 5 hr had a hazard ratio = 1.54 (95% confidence interval = 1.32–1.80), while the corresponding hazard ratio was 1.05 (95% confidence interval = 0.88–1.27) for men, the interaction being significant (p < 0.05). For cardiovascular disease mortality, exclusion of the first 2 years of exposure, as well as competing risk analysis eliminated the originally significant interaction. Cancer mortality did not show any significant interaction. Survival analysis of the difference between the reference duration (6 hr) and the short duration (< 5 hr) during follow-up showed a gradually steeper reduction of survival time for women than for men for all-cause mortality. We also observed that the lowest cancer mortality appeared for the 5-hr sleep duration. In conclusion, the pattern of association between short sleep duration and all-cause mortality differed between women and men, and the difference between men and women increased with follow-up time.

Sleep restriction therapy is a central component of cognitive behavioural therapy for insomnia, but can lead to excessive sleepiness, which may impede treatment adherence. Sleep compression therapy has been suggested as a possibly gentler alternative. The aim of this study was to compare the effects of sleep restriction therapy and sleep compression therapy on objective measures of sleep, with a focus on magnitude and timing of effects. From a larger study of participants with insomnia, a sub-sample of 36 underwent polysomnographic recordings, before being randomised to either sleep restriction (n = 19) or sleep compression (n = 17) and receiving online treatment for 10 weeks. Assessments with polysomnography were also carried out after 2, 5, and 10 weeks of treatment. Data were analysed with multilevel linear mixed effect modelling. As per treatment instructions, participants in sleep restriction initially spent shorter time in bed compared with sleep compression. Participants in sleep restriction also showed an initial decrease of total sleep time, which was not seen in the sleep compression group. Both treatments led to improvements in sleep continuity variables, with a tendency for the improvements to come earlier during treatment in sleep restriction. No substantial differences were found between the two treatments 10 weeks after the treatment start. The results indicate that homeostatic sleep pressure may not be as important as a mechanism in sleep compression therapy as in sleep restriction therapy, and an investigation of other mechanisms is needed. In conclusion, the treatments led to similar changes in objective sleep at a somewhat different pace, and possibly through different mechanisms.