Insomnia, the most prevalent sleep disorder worldwide, confers marked risks for both physical and mental health. Furthermore, insomnia is associated with considerable direct and indirect healthcare costs. Recent guidelines in the US and Europe unequivocally conclude that cognitive behavioural therapy for insomnia (CBT-I) should be the first-line treatment for the disorder. Current treatment approaches are in stark contrast to these clear recommendations, not least across Europe, where, if any treatment at all is delivered, hypnotic medication still is the dominant therapeutic modality. To address this situation, a Task Force of the European Sleep Research Society and the European Insomnia Network met in May 2018. The Task Force proposed establishing a European CBT-I Academy that would enable a Europe-wide system of standardized CBT-I training and training centre accreditation. This article summarizes the deliberations of the Task Force concerning definition and ingredients of CBT-I, preconditions for health professionals to teach CBT-I, the way in which CBT-I should be taught, who should be taught CBT-I and to whom CBT-I should be administered. Furthermore, diverse aspects of CBT-I care and delivery were discussed and incorporated into a stepped-care model for insomnia.
Obstructive sleep apnea leads to recurrent arousals from sleep, oxygen desaturations, daytime sleepiness and fatigue. This can have an adverse impact on quality of life. The aims of this study were to compare: (i) quality of life between the general population and untreated patients with obstructive sleep apnea; and (ii) changes of quality of life among patients with obstructive sleep apnea after 2 years of positive airway pressure treatment between adherent patients and non-users. Propensity score methodologies were used in order to minimize selection bias and strengthen causal inferences. The enrolled obstructive sleep apnea subjects (n = 822) were newly diagnosed with moderate to severe obstructive sleep apnea who were starting positive airway pressure treatment, and the general population subjects (n = 742) were randomly selected Icelanders. The Short Form 12 was used to measure quality of life. Untreated patients with obstructive sleep apnea had a worse quality of life when compared with the general population. This effect remained significant after using propensity scores to select samples, balanced with regard to age, body mass index, gender, smoking, diabetes, hypertension and cardiovascular disease. We did not find significant overall differences between full and non-users of positive airway pressure in improvement of quality of life from baseline to follow-up. However, there was a trend towards more improvement in physical quality of life for positive airway pressure-adherent patients, and the most obese subjects improved their physical quality of life more. The results suggest that co-morbidities of obstructive sleep apnea, such as obesity, insomnia and daytime sleepiness, have a great effect on life qualities and need to be taken into account and addressed with additional interventions.
Insomnia and obstructive sleep apnea (OSA) often coexist, but the nature of their relationship is unclear. The aims of this study were to compare the prevalence of initial and middle insomnia between OSA patients and controls from the general population as well as to study the influence of insomnia on sleepiness and quality of life in OSA patients. Two groups were compared, untreated OSA patients (n = 824) and controls ≥ 40 years from the general population in Iceland (n = 762). All subjects answered the same questionnaires on health and sleep and OSA patients underwent a sleep study. Altogether, 53% of controls were males compared to 81% of OSA patients. Difficulties maintaining sleep (DMS) were more common among men and women with OSA compared to the general population (52 versus 31% and 62 versus 31%, respectively, P < 0.0001). Difficulties initiating sleep (DIS) and DIS + DMS were more common among women with OSA compared to women without OSA. OSA patients with DMS were sleepier than patients without DMS (Epworth Sleepiness Scale: 12.2 versus 10.9, P < 0.001), while both DMS and DIS were related to lower quality of life in OSA patients as measured by the Short Form 12 (physical score 39 versus 42 and mental score 36 versus 41, P < 0.001). DIS and DMS were not related to OSA severity. Insomnia is common among OSA patients and has a negative influence on quality of life and sleepiness in this patient group. It is relevant to screen for insomnia among OSA patients and treat both conditions when they co-occur.
The association between nightmare frequency (NMF) and suicidal ideation (SI) is well known, yet the impact of the COVID-19 pandemic on this relation is inconsistent. This study aimed to investigate changes in NMF, SI, and their association during the COVID-19 pandemic. Data were collected in 16 countries using a harmonised questionnaire. The sample included 9328 individuals (4848 women; age M[SD] = 46.85 [17.75] years), and 17.60% reported previous COVID-19. Overall, SI was significantly 2% lower during the pandemic vs. before, and this was consistent across genders and ages. Most countries/regions demonstrated decreases in SI during this pandemic, with Austria (-9.57%), Sweden (-6.18%), and Bulgaria (-5.14%) exhibiting significant declines in SI, but Italy (1.45%) and Portugal (2.45%) demonstrated non-significant increases. Suicidal ideation was more common in participants with long-COVID (21.10%) vs. short-COVID (12.40%), though SI did not vary by COVID-19 history. Nightmare frequency increased by 4.50% during the pandemic and was significantly higher in those with previous COVID-19 (14.50% vs. 10.70%), during infection (23.00% vs. 8.10%), and in those with long-COVID (18.00% vs. 8.50%). The relation between NMF and SI was not significantly stronger during the pandemic than prior (rs = 0.18 vs. 0.14; z = 2.80). Frequent nightmares during the pandemic increased the likelihood of reporting SI (OR = 1.57, 95% CI 1.20-2.05), while frequent dream recall during the pandemic served a protective effect (OR = 0.74, 95% CI 0.59-0.94). These findings have important implications for identifying those at risk of suicide and may offer a potential pathway for suicide prevention.
Chronic insomnia is a prevalent problem in primary health care and tends to be more serious than insomnia in the general population. These patients often obtain little benefit from hypnotics, and are frequently open to exploring various options for medical treatment. However, most general practitioners (GPs) are unable to provide such options. Several meta-analyses have shown that cognitive-behavioural therapy (CBT) for insomnia results in solid improvements on sleep parameters, and a few studies have demonstrated promising results for nurse-administered CBT in primary care. The aim of this randomized controlled study was to investigate the clinical effectiveness of manual-guided CBT for insomnia delivered by ordinary primary care personnel in general medical practice with unselected patients. Sixty-six primary care patients with insomnia were randomized to CBT or a waiting-list control group. The CBT group improved significantly more than the control group using the Insomnia Severity Index as the outcome. The effect size was high. Sleep diaries showed a significant, medium-sized treatment effect for sleep onset latency and wake time after sleep onset. However, for all measures there is a marked deterioration at follow-up assessments. Almost half of the treated subjects (47%) reported a clinically relevant treatment effect directly after treatment. It is concluded that this way of delivering treatment may be cost-effective.
The hormone fibroblast growth factor 21 (FGF21) modulates tissue metabolism and circulates at higher levels in metabolic conditions associated with chronic sleep-wake disruption, such as type 2 diabetes and obesity. In the present study, we investigated whether acute sleep loss impacts circulating levels of FGF21 and tissue-specific production, and response pathways linked to FGF21. A total of 15 healthy normal-weight young men participated in a randomised crossover study with two conditions, sleep loss versus an 8.5-hr sleep window. The evening before each intervention, fasting blood was collected. Fasting, post-intervention morning skeletal muscle and adipose tissue samples underwent quantitative polymerase chain reaction and DNA methylation analyses, and serum FGF21 levels were measured before and after an oral glucose tolerance test. Serum levels of FGF21 were higher after sleep loss compared with sleep, both under fasting conditions and following glucose intake (~27%-30%, p = 0.023). Fasting circulating levels of fibroblast activation protein, a protein which can degrade circulating FGF21, were not altered by sleep loss, whereas DNA methylation in the FGF21 promoter region increased only in adipose tissue. However, even though specifically the muscle exhibited transcriptional changes indicating adverse alterations to redox and metabolic homeostasis, no tissue-based changes were observed in expression of FGF21, its receptors, or selected signalling targets, in response to sleep loss. In summary, we found that acute sleep loss resulted in increased circulating levels of FGF21 in healthy young men, which may occur independent of a tissue-based stress response in metabolic peripheral tissues. Further studies may decipher whether changes in FGF21 signalling after sleep loss modulate metabolic outcomes associated with sleep or circadian disruption.
The present study sought to investigate whether a single night of partial sleep deprivation (PSD) would alter fasting insulin sensitivity and cephalic phase insulin release (CPIR) in humans. A rise in circulating insulin in response to food-related sensory stimulation may prepare tissues to break down ingested glucose, e.g. by stimulating rate-limiting glycolytic enzymes. In addition, given insulin's anorexigenic properties once it reaches the brain, the CPIR may serve as an early peripheral satiety signal. Against this background, in the present study 16 men participated in two separate sessions: one night of PSD (4.25 h sleep) versus one night of full sleep (8.5 h sleep). In the morning following each sleep condition, subjects' oral cavities were rinsed with a 1-molar sucrose solution for 45 s, preceded and followed by blood sampling for repeated determination of plasma glucose and serum insulin concentrations (-3, +3, +5, +7, +10 and +20 min). Our main result was that PSD, compared with full sleep, was associated with significantly higher peripheral insulin resistance, as indicated by a higher fasting homeostasis model assessment of insulin resistance index (+16%, P = 0.025). In contrast, no CPIR was observed in any of the two sleep conditions. Our findings indicate that a single night of PSD is already sufficient to impair fasting insulin sensitivity in healthy men. In contrast, brief oral cavity rinsing with sucrose solution did not change serum insulin concentrations, suggesting that a blunted CPIR is an unlikely mechanism through which acute sleep loss causes metabolic perturbations during morning hours in humans.
Acute sleep loss influences visual processes in humans, such as recognizing facial emotions. However, to the best of our knowledge, no study till date has examined whether acute sleep loss alters visual comfort when looking at images. One image statistic that can be used to investigate the level of visual comfort experienced under visual encoding is the slope of the amplitude spectrum, also referred to as the slope constant. The slope constant describes the spatial distribution of pixel intensities and deviations from the natural slope constant can induce visual discomfort. In the present counterbalanced crossover design study, 11 young men with normal or corrected-to-normal vision participated in two experimental conditions: one night of sleep loss and one night of sleep. In the morning after each intervention, subjects performed a computerized psychophysics task. Specifically, they were required to adjust the slope constant of images depicting natural landscapes and close-ups with a randomly chosen initial slope constant until they perceived each image as most natural looking. Subjects also rated the pleasantness of each selected image. Our analysis showed that following sleep loss, higher slope constants were perceived as most natural looking when viewing images of natural landscapes. Images with a higher slope constant are generally perceived as blurrier. The selected images were also rated as less pleasant after sleep loss. No such differences between the experimental conditions were noted for images of close-ups. The results suggest that sleep loss induces signs of visual discomfort in young men. Possible implications of these findings are discussed.
Previous studies have indicated involvement of the thalamus and the pons in Kleine-Levin syndrome. In the present study, functional connectivity of the thalamus and the pons was investigated in asymptomatic patients with Kleine-Levin syndrome and healthy controls. Twelve patients and 14 healthy controls were investigated by functional magnetic resonance imaging during rest. Resting state images were analysed using seed regions of interest in the thalamus and the pons. The results showed significantly lower functional connectivity between the pons and the frontal eye field in persons with Kleine-Levin syndrome compared with healthy controls. There were no connectivity differences involving the thalamus. Based on these findings, a relation is proposed between the sleep disorder Kleine-Levin syndrome and cerebral control of eye movements, which in turn is related to visual attention and working memory. This hypothesis has to be tested in future studies of oculomotor control in Kleine-Levin syndrome.
PAX6 gene mutations cause a variety of eye and central nervous system (CNS) abnormalities. Aniridia is often accompanied by CNS abnormalities such as pineal gland atrophy or hypoplasia, leading to disturbed circadian rhythm and sleep disorders. Less is known on the coincidence of narcolepsy in this patient group. We aimed to find out whether the circadian rhythm or sleep-wake structure was affected in patients with aniridia. Four members of a family segregating with congenital aniridia in two generations were included in the study. The patients were subjected to genetic testing for a PAX6 mutation, multiple sleep latency test, whole-brain magnetic resonance imaging (MRI), hypocretin-1 in cerebrospinal fluid, and Human Leukocyte Antigen DQ beta1*06:02. All four members were heterozygous for the pathogenic c.959-1G>A mutation in the PAX6 gene. Sleep disturbance was observed in all family members. The index patient was diagnosed with narcolepsy. MRI showed a hypoplastic pineal gland in all members. We describe the first case of a patient with PAX6 haploinsufficiency, aniridia and pineal gland hypoplasia diagnosed with narcolepsy type-1, suggesting a complex sleep disorder pathogenesis.
Systemic inflammation is thought to mediate the link between sleep and cardiovascular outcomes, but previous studies on sleep habits and inflammation markers have found inconsistent results. This study investigated the relationship between sleep characteristics and C-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor α (TNFα). A representative sample of 319 Swedish women was randomly selected from the general population for in-home polysomnography, sleep questionnaire and blood samples. As variables were highly correlated, principal component analysis was used to reduce the number of original variables. Linear regression with log-transformation of the outcomes (lnCRP, lnIL-6 and lnTNFα) and quantile regression were fitted to estimate cross-sectional relationships. Multivariable linear regression models suggested a significant association of insomnia symptoms (self-reported) with higher lnCRP levels (β = 0.11; 95% confidence interval [CI] = 0.02; 0.21), but not with lnIL-6 and lnTNFα. From quantile regression analysis we found that a high non-restorative index (subjective) and insomnia symptoms (self-reported) were associated with higher values of CRP, especially in the highest quantiles of the CRP distribution (90th percentile: β = 0.71; 95% CI = 0.17; 1.24. β = 1.23; 95% CI = 0.44; 2.02, respectively). Additionally, higher amounts of rapid eye movement (REM) sleep were associated with lower CRP values (90th percentile: β = -0.80; 95% CI = -0.14; -1.46). In conclusion, sleep disturbances (self-reported), specifically difficulties maintaining sleep and early morning awakenings, but not sleep duration (neither subjective nor objective), were associated with higher CRP levels. No association was found with IL-6 or TNFα. Elevated REM sleep was associated with lower CRP levels. The results suggest that inflammation might be an intermediate mechanism linking sleep and health in women.
The aim of this work was to evaluate the measurement properties and hierarchical item structure of the Epworth Sleepiness Scale (ESS) in patients with Parkinson's disease (PD). Data were taken from a cross-sectional study regarding fatigue and sleep-related aspects of PD. One hundred and eighteen consecutive patients with neurologist-diagnosed PD without significant co-morbidities (54% men; mean age, 64 years; mean PD duration, 8.4 years) from four Swedish neurological outpatient clinics participated. The ESS displayed good data quality with few missing items (0–2.5%): good reliability (Cronbach's alpha, 0.84), marginal floor and no ceiling effects (1.7% and 0% respectively), and differentiated between those reporting problems staying awake during the past month and those who did not. Item–total correlations, factor and Rasch analyses indicated that items tap a single underlying construct. Rasch analysis supported basic rating scale assumptions and demonstrated an item hierarchy similar to that previously found in patients with other sleep disorders. Gaps in the levels of sleep propensity covered by ESS items and their response options were identified at the higher and lower ends of the underlying sleepiness continuum. This study provides an evidence base for using the ESS in PD by demonstrating good psychometric properties and a stable hierarchical item structure. However, addition of new items and use of Rasch scoring has potential to further enhance the clinical usefulness of the ESS.
Obstructive sleep apnea (OSA) may lead to increased circulating concentrations of inflammatory biomarkers and treatment may change these. We aimed to assess the effect of oral appliance (OA) therapy on inflammatory biomarkers in a randomised controlled pilot trial. A total of 71 patients with OSA and systemic hypertension were randomly allocated to an active, mandible protruded (OAa) or a passive, mandible non-protruded device (OAp) treatment. Serum concentrations of the inflammatory biomarkers white blood cells, high-sensitivity C-reactive protein, interleukin 6, interleukin 10, and tumour necrosis factor-alpha were measured at baseline and after 3 months of OA treatment. The differences between treatment groups in biomarker concentration change during the treatment were presented as the Vargha and Delaney effect size and evaluated with the Wilcoxon-Mann-Whitney test. This effect size expresses the probability of a higher value in a random participant from one group compared with a random patient from the other group, and a value of 0.5 means stochastically equal groups. After 3 months of treatment, there was a significant reduction of the apnea-hypopnea index in the OAa group compared with the OAp group (effect size 0.258, 95% confidence interval 0.146-0.386, p < .001). There were no significant differences between the groups in any of the inflammatory markers' concentration changes during the treatment period (effect sizes between 0.488 and 0.524; all p values >=.737). Thus, OA treatment for 3 months did not affect circulating concentrations of some common inflammatory markers in patients with OSA and systemic hypertension.
The study investigated the association between onset of workplace violence and onset of sleep disturbances. We used self-reported data from the Swedish Longitudinal Occupational Survey of Health (SLOSH) collected in 2014, 2016, and 2018. A two-wave design was based on participants who had no exposure to workplace violence or sleep disturbances at baseline (n = 6,928). A three-wave design was based on participants who in addition were unexposed to sleep disturbances in the second wave (n = 6,150). Four items of the Karolinska Sleep Questionnaire were used to measure sleep disturbances and one question was used to measure the occurrence of workplace violence or threats of violence. Multivariate logistic regression analyses were performed. In the two-wave approach, onset of workplace violence was associated with onset of sleep disturbances after adjustment for sex, age, occupational position, education, and civil status (adjusted odds ratio 1.41, 95% confidence interval 1.02-1.96). The association was no longer statistically significant after further adjustment for night/evening work, demands, control, and social support at work. In the three-wave approach, results were only suggestive of an association between onset of workplace violence and subsequent onset of sleep disturbances after adjustment for sex, age, occupational position, education, and civil status. Onset of frequent exposure to workplace violence was associated with subsequent onset of sleep disturbances in the adjusted analyses, but these analyses were based on few individuals (13 exposed versus 5,907 unexposed). The results did not conclusively demonstrate that onset of workplace violence predicts development of sleep disturbances. Further research could elucidate the role of other working conditions.
Accelerometers placed on the thigh provide accurate measures of daily physical activity types, postures and sedentary behaviours, over 24 h and across consecutive days. However, the ability to estimate sleep duration or quality from thigh-worn accelerometers is uncertain and has not been evaluated in comparison with the ‘gold-standard’ measurement of sleep polysomnography. This study aimed to develop an algorithm for sleep estimation using the raw data from a thigh-worn accelerometer and to evaluate it in comparison with polysomnography. The algorithm was developed and optimised on a dataset consisting of 23 single-night polysomnography recordings, collected in a laboratory, from 15 asymptomatic adults. This optimised algorithm was then applied to a separate evaluation dataset, in which, 71 adult males (mean [SD] age 57 [11] years, height 181 [6] cm, weight 82 [13] kg) wore ambulatory polysomnography equipment and a thigh-worn accelerometer, simultaneously, whilst sleeping at home. Compared with polysomnography, the algorithm had a sensitivity of 0.84 and a specificity of 0.55 when estimating sleep periods. Sleep intervals were underestimated by 21 min (130 min, Limits of Agreement Range [LoAR]). Total sleep time was underestimated by 32 min (233 min LoAR). Our results evaluate the performance of a new algorithm for estimating sleep and outline the limitations. Based on these results, we conclude that a single device can provide estimates of the sleep interval and total sleep time with sufficient accuracy for the measurement of daily physical activity, sedentary behaviour, and sleep, on a group level in free-living settings.
Chronic insomnia is a common and burdensome problem for patients seeking primary care. Cognitive behavioural therapy has been shown to be effective for insomnia, also when presented with co-morbidities, but access to sleep therapists is limited. Group-treatment and self-administered treatment via self-help books have both been shown to be efficacious treatment options, and the present study aimed to evaluate the effect of an open-ended group intervention based on a self-help book for insomnia, adapted to fit a primary-care setting. Forty primary-care patients with insomnia (mean age 55 years, 80% women) were randomized to the open-ended group intervention based on a cognitive behavioural therapy for insomnia self-help book or to a care as usual/wait-list control condition. Results show high attendance to group sessions and high treatment satisfaction. Participants in the control group later received the self-help book, but without the group intervention. The book-based group treatment resulted in significantly improved insomnia severity, as well as shorter sleep-onset latency, less wake time after sleep onset, and less use of sleep medication compared with treatment as usual. The improvements were sustained at a 4-year follow-up assessment. A secondary analysis found a significant advantage of the combination of the book and the open-ended group intervention compared with when the initial control group later used only the self-help book. An open-ended treatment group based on a self-help book for insomnia thus seems to be an effective and feasible intervention for chronic insomnia in primary-care settings.
Rapid eye movement (REM) obstructive sleep apnea might be particularly harmful to the cardiovascular system. We aimed to investigate the association between sleep apnea during REM sleep and signs of atherosclerotic disease in the form of carotid intima thickness in a community-based sample of men and women and possible sex differences in this association. The association between sleep apnea during REM sleep and intima thickness was analysed cross-sectionally in women from the community-based "Sleep and Health in Women" (SHE) study (n = 253) and age- and body mass index (BMI)-matched men from the "Men in Uppsala; a Study of sleep, Apnea and Cardiometabolic Health" (MUSTACHE) study (n = 338). Confounders adjusted for were age, BMI, gender, alcohol, and smoking. All participants underwent a full-night polysomnography, high-resolution ultrasonography of the common carotid artery, anthropometric measurements, blood pressure measurements, and answered questionnaires. There was an association between sleep apnea during REM sleep and thicker carotid intima that remained after adjustment for confounding (adjusted β = 0.008, p = 0.032). The intima was increased by 9.9% in the group with severe sleep apnea during REM sleep, and this association between severe sleep apnea during REM sleep and increased intima thickness remained after adjustment for confounders (adjusted β = 0.043, p = 0.021). More women than men had severe sleep apnea during REM sleep; moreover, in sex-stratified analyses, the association between sleep apnea during REM sleep and intima thickness was found in women but not in men. We conclude that severe REM sleep apnea is independently associated with signs of atherosclerosis. When stratified by sex, the association is seen in women but not in men.
Proteomic-based technologies offer new opportunities to identify proteins that might reflect the cardiometabolic stress caused by different aspects of sleep-disordered breathing. We aimed to investigate whether severe obstructive sleep apnea and severe obstructive sleep apnea during rapid eye movement sleep are associated with changed levels of inflammatory and cardiac disease-related proteins in a population-based cohort of women. In the community-based "Sleep and Health in Women" (SHE) cohort study, 400 women underwent polysomnography, anthropometric measurements and blood sampling. Two proteomic assays (Olink Proseek(R)Inflammation panel and Olink Proseek(R)Cardiovascular II panel), each measuring 92 proteins, were analysed in a subsample of 253 women.p-Values were adjusted for multiple testing, with false discovery rate set at 10%. In unadjusted models, 57 proteins were associated with apnea-hypopnea index, 56 proteins with oxygen desaturation index and 64 proteins with rapid eye movement-apnea-hypopnea index. After adjustment for age, body mass index and plate, there were no significant associations between apnea-hypopnea index or oxygen desaturation index and any of the proteins. Severe obstructive sleep apnea during rapid eye movement sleep (rapid eye movement-apnea-hypopnea index >= 30) was associated with decreased levels of two anti-inflammatory proteins; Sirt2 (q-value .016) and LAP-TGF-beta(1)(q-value .016). There was also a negative association between rapid eye movement-apnea-hypopnea index of >= 30 and Axin1 (q-value .095), a protein thought to facilitate TGF-beta-signalling. We conclude that severe obstructive sleep apnea during rapid eye movement sleep is associated with low levels of Sirt2, LAP-TGF-beta(1)and Axin1, anti-inflammatory proteins involved in metabolic regulation and in the atherosclerotic process. For obstructive sleep apnea based on a whole night, the associations with cardiac and inflammatory proteins are weaker, and explained to a large extent by age and body mass index.
Many people report suffering from post-acute sequelae of COVID-19 or "long-COVID", but there are still open questions on what actually constitutes long-COVID and how prevalent it is. The current definition of post-acute sequelae of COVID-19 is based on voting using the Delphi-method by the WHO post-COVID-19 working group. It emphasizes long-lasting fatigue, shortness of breath and cognitive dysfunction as the core symptoms of post-acute sequelae of COVID-19. In this international survey study consisting of 13,628 subjects aged 18-99 years from 16 countries of Asia, Europe, North America and South America (May-Dec 2021), we show that post-acute sequelae of COVID-19 symptoms were more prevalent amongst the more severe COVID-19 cases, i.e. those requiring hospitalisation for COVID-19. We also found that long-lasting sleep symptoms are at the core of post-acute sequelae of COVID-19 and associate with the COVID-19 severity when COVID-19 cases are compared with COVID-negative cases. Specifically, fatigue (61.3%), insomnia symptoms (49.6%) and excessive daytime sleepiness (35.8%) were highly prevalent amongst respondents reporting long-lasting symptoms after hospitalisation for COVID-19. Understanding the importance of sleep-related symptoms in post-acute sequelae of COVID-19 has a clinical relevance when diagnosing and treating long-COVID.
Weighted blankets have emerged as a potential non-pharmacological intervention to ease conditions such as insomnia and anxiety. Despite a lack of experimental evidence, these alleged effects are frequently attributed to a reduced activity of the endogenous stress systems and an increased release of hormones such as oxytocin and melatonin. Thus, the aim of the present in-laboratory crossover study (26 young and healthy participants, including 15 men and 11 women) was to investigate if using a weighted blanket (~12% of body weight) at bedtime resulted in higher salivary concentrations of melatonin and oxytocin compared with a light blanket (~2.4% of body weight). We also examined possible differences in salivary concentrations of the stress hormone cortisol, salivary alpha-amylase activity (as an indicative metric of sympathetic nervous system activity), subjective sleepiness, and sleep duration. When using a weighted blanket, the 1 hour increase of salivary melatonin from baseline (i.e., 22:00) to lights off (i.e., 23:00) was about 32% higher (p = 0.011). No other significant differences were found between the blanket conditions, including subjective sleepiness and total sleep duration. Our study is the first to suggest that using a weighted blanket may result in a more significant release of melatonin at bedtime. Future studies should investigate whether the stimulatory effect on melatonin secretion is observed on a nightly basis when frequently using a weighted blanket over weeks to months. It remains to be determined whether the observed increase in melatonin may be therapeutically relevant for the previously described effects of the weighted blanket on insomnia and anxiety.
Consumer sleep wearables are increasingly popular, even among patients with sleep problems. However, the daily feedback provided by these devices could exacerbate sleep-related worry. To investigate this issue, 14 patients received a self-help guide booklet to improve sleep and wore the sleep tracker Fitbit Inspire 2 on their non-dominant hand for 4 weeks, while a control group of 12 patients only kept a handwritten sleep diary. All patients completed questionnaires at a primary care centre's first and final visit to assess general anxiety, sleep quality, sleep reactivity to stress, and quality of life. Our analysis showed that sleep quality, sleep reactivity to stress, and quality of life improved significantly for all patients between the first and final visit (p < 0.05). However, there were no significant differences between the Fitbit and control groups. Using sleep diary-derived estimates from the first and last week, we found that the control group but not the Fitbit group, increased their average time asleep each night and sleep efficiency (p < 0.05). However, these differences were primarily driven by baseline differences between the two groups. Our findings suggest that using wearables does not necessarily exacerbate sleep worries among people with insomnia.
Growing evidence indicates that retiring from paid work is associated, at least in the short-term, with dramatic reductions in sleep difficulties and more restorative sleep. However, much is still not known, in particular how universal these improvements are, how long they last, and whether they relate to the work environment. A methodological challenge concerns how to model time when studying abrupt changes such as retirement. Using data from Swedish Longitudinal Occupational Survey of Health (n = 2,148), we studied difficulties falling asleep, difficulties maintaining sleep, premature awakening, restless sleep, a composite scale of these items, and non-restorative sleep. We compared polynomial and B-spline functions to model time in group-based trajectory modelling. We estimated variations in the individual development of sleep difficulties around retirement, relating these to the pre-retirement work environment. Reductions in sleep difficulties at retirement were sudden for all outcomes and were sustained for up to 11 years for non-restorative sleep, premature awakening, and restless sleep. Average patterns masked distinct patterns of change: groups of retirees experiencing greatest pre-retirement sleep difficulties benefitted most from retiring. Higher job demands, lower work time control, lower job control, and working full-time were work factors that accounted membership in these groups. Compared to polynomials, B-spline models more appropriately estimated time around retirement, providing trajectories that were closer to the observed shapes. The study highlights the need to exercise care in modelling time over a sudden transition because using polynomials can generate artefactual uplifts or omit abrupt changes entirely, findings that would have fallacious implications.
Acute sleep deprivation can lead to judgement errors and thereby increases the risk of accidents, possibly due to an impaired working memory. However, whether the adverse effects of acute sleep loss on working memory are modulated by auditory distraction in women and men are not known. Additionally, it is unknown whether sleep loss alters the way in which men and women perceive their working memory performance. Thus, 24 young adults (12 women using oral contraceptives at the time of investigation) participated in two experimental conditions: nocturnal sleep (scheduled between 22:30 and 06:30 hours) versus one night of total sleep loss. Participants were administered a digital working memory test in which eight-digit sequences were learned and retrieved in the morning after each condition. Learning of digital sequences was accompanied by either silence or auditory distraction (equal distribution among trials). After sequence retrieval, each trial ended with a question regarding how certain participants were of the correctness of their response, as a self-estimate of working memory performance. We found that sleep loss impaired objective but not self-estimated working memory performance in women. In contrast, both measures remained unaffected by sleep loss in men. Auditory distraction impaired working memory performance, without modulation by sleep loss or sex. Being unaware of cognitive limitations when sleep-deprived, as seen in our study, could lead to undesirable consequences in, for example, an occupational context. Our findings suggest that sleep-deprived young women are at particular risk for overestimating their working memory performance.
It is well known that the quantity and quality of physiological sleep changes across age. However, so far the effect of age on sleep microstructure has been mostly addressed in small samples. The current study examines the effect of age on several measures of sleep macro- and microstructure in 211 women (22-71years old) of the Sleep and Health in Women' study for whom ambulatory polysomnography was registered. Older age was associated with significantly lower fast spindle (effect size f(2)=0.32) and K-complex density (f(2)=0.19) during N2 sleep, as well as slow-wave activity (log) in N3 sleep (f(2)=0.21). Moreover, total sleep time (f(2)=0.10), N3 sleep (min) (f(2)=0.10), rapid eye movement sleep (min) (f(2)=0.11) and sigma (log) (f(2)=0.05) and slow-wave activity (log) during non-rapid eye movement sleep (f(2)=0.09) were reduced, and N1 sleep (f(2)=0.03) was increased in older age. No significant effects of age were observed on slow spindle density, rapid eye movement density and beta power (log) during non-rapid eye movement sleep. In conclusion, effect sizes indicate that traditional sleep stage scoring may underestimate age-related changes in sleep.