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Background: Large electricity-generating wind turbines emit both audible sound and inaudible infrasound at very low frequencies that are outside of the normal human range of hearing. Sufferers of wind turbine syndrome (WTS) have attributed their ill-health and particularly their sleep disturbance to the signature pattern of infrasound. Critics have argued that these symptoms are psychological in origin and are attributable to nocebo effects. Objectives: We aimed to test the effects of 72 h of infrasound (1.6-20 Hz at a sound level of ~ 90 dB pk re 20 pPa, simulating a wind turbine infrasound signature) exposure on human physiology, particularly sleep. Methods: We conducted a randomized double-blind triple-arm crossover laboratory-based study of 72 h exposure with a >10-d washout conducted in a noise-insulated sleep laboratory in the style of a studio apartment. The exposures were infrasound (~90 dB pk), sham infrasound (same speakers not generating infrasound), and traffic noise exposure [active control; at a sound pressure level of 40-50 dB L[A.sub.eq,night] and 70 dB LA[F.sub.max] transient maxima, night (2200 to 0700 hours)]. The following physiological and psychological measures and systems were tested for their sensitivity to infrasound: wake after sleep onset (WASO; primary outcome) and other measures of sleep physiology, wake electroencephalography, WTS symptoms, cardiovascular physiology, and neurobehavioral performance. Results: We randomized 37 noise-sensitive but otherwise healthy adults (18-72 years of age; 51% female) into the study before a COVID19-related public health order forced the study to close. WASO was not affected by infrasound compared with sham infrasound (-1.36 min; 95% CI: -6.60, 3.88, p = 0.60) but was worsened by the active control traffic exposure compared with sham by 6.07 min (95% CI: 0.75, 11.39, p = 0.02). Infrasound did not worsen any subjective or objective measures used. Discussion: Our findings did not support the idea that infrasound causes WTS. High level, but inaudible, infrasound did not appear to perturb any physiological or psychological measure tested in these study participants. https://doi.org/10.1289/EHP10757, Introduction Large electricity-generating wind turbines emit both audible sound and inaudible infrasound at very low frequencies that are outside of the normal human range of hearing. There have been several [...]

This study assessed whether the addition of continuous positive airway pressure (CPAP) during weight loss would enhance cardiometabolic health improvements in patients with obesity and Obstructive Sleep Apnoea (OSA). Patients with overweight or obesity, pre-diabetes and moderatesevere OSA were randomised to receive CPAP therapy with a weight loss programme (CPAP+WL) or a weight loss programme alone (WL alone). Primary outcome: 2-hour glucose assessed by an oral glucose tolerance test. Secondary outcomes: 24 hr blood pressure, body composition (DEXA) and fasting blood markers. 17 patients completed 3-month follow-up assessments (8 CPAP+WL and 9 WL alone). Overall, participants in both groups lost ∼12 kg which reduced polysomnography determined OSA severity by ∼45 %. In the CPAP+WL group, CPAP use (compliance 5.29 hrs/night) did not improve any outcome above WL alone. There was no improvement in 2-hour glucose in either group. However, in the pooled (n = 17) analysis there were overall improvements in most outcomes including insulin sensitivity (.000965 units, p =.008), sleep systolic BP (- 16.2 mmHg, p =.0003), sleep diastolic BP (−9.8 mmHg, p = 0.02), wake diastolic BP (- 4.3 mmHg, p =.03) and sleepiness (Epworth Sleepiness Score −3.2, p =.0003). In addition, there were reductions in glucose area under the curve (−230 units, p =.009), total (−0.86 mmol/L, p = 0.006) and LDL cholesterol (−0.58 mmol/L, p = 0.007), triglycerides (−0.75 mmol/L, p = 0.004), fat mass (−7.6 kg, p <.0001) and abdominal fat (−310 cm3, p <.0001). Weight loss reduced OSA and improved sleepiness and cardiometabolic health. These improvements were not further enhanced by using CPAP. Results suggest weight loss should be the primary focus of treatment for patients with OSA and obesity. [ABSTRACT FROM AUTHOR]

Summary: Our objective was to assess the agreement and linear relationships amongst multiple measures of sleep duration in a sample of patients with insomnia disorder and good sleeper controls. We retrospectively analysed data from 123 patients with insomnia disorder and 123 age‐ and gender‐matched good sleeper controls who completed a simple subjective habitual sleep duration question (Pittsburgh Sleep Quality Index), a sleep diary (5–14 days), 2 nights of polysomnography, and two corresponding morning subjective estimates of sleep duration. Descriptive statistics, linear regression analyses and Bland–Altman plots were used to describe the relationship and (dis)agreement between sleep duration measures. Relationships between polysomnography and the simple question as well as between polysomnography and sleep diary were weak to non‐existent. Subjective measures and polysomnography did not agree. Sleep duration measured with the Pittsburgh Sleep Quality Index or sleep diary was about 2 hr above or up to 4 hr below polysomnography‐measured sleep duration. Patients with insomnia disorder, on average, reported shorter sleep duration compared with polysomnography, while good sleeper controls, on average, reported longer sleep duration compared with polysomnography. The results suggest that subjective and objective measures apparently capture different aspects of sleep, even when nominally addressing the same value (sleep duration). They disagree in both patients with insomnia disorder and good sleeper controls, but in different directions. Studies assessing sleep duration should take into account both the investigated population and the assessment method when interpreting results. Future studies should continue to investigate possible psychological and physiological correlates of sleep (mis)perception. [ABSTRACT FROM AUTHOR]

Summary: Sleep restriction therapy (SRT) is an effective stand‐alone behavioural intervention for insomnia disorder. However, its daytime side effects, particularly sleepiness, may be troubling for patients and/or may be a necessary part of the patient's treatment journey. This pilot trial aims to explore the potential benefit of armodafinil, a wakefulness promoter. Patients were treated with SRT with open label adjunctive armodafinil (150 mg/day). Thirty‐three patients from previous studies that have undergone exactly the same SRT intervention acted as controls. The primary outcome measure was the insomnia severity index (ISI), and secondary outcomes were the Epworth sleepiness scale, sleep restriction adherence scale (SRAS), and safety from baseline through to 12 weeks. We recruited 25 patients into the trial. Data for the primary end point (ISI at 12 weeks) was available for 20 of the participants. The baseline insomnia severity index was 20.2 (SD 3.3) and decreased to 9.1 (SE 1.1), with no change, to 10.2 and 11.2 at weeks 6 and 12 respectively (all p > 0.05 compared with baseline). The insomnia severity index values for armodafinil patients were statistically inferior to historical controls at the primary time point of 12 weeks (11.2 vs. 6.7, p < 0.01). Sleep restriction therapy plus armodafinil treatment was associated with frequent minor side effects but was generally safe and acceptable to patients. Sleep restriction therapy was associated with a robust clinical response in the insomnia severity index values for insomnia patients. Based upon historical control data, armodafinil does not appear to have beneficial adjunctive effects in addition to sleep restriction therapy alone. [ABSTRACT FROM AUTHOR]

The article focuses on the association between obstructive sleep apnea (OSA) and cardiovascular events. Topics include the lack of cardiovascular event reduction with continuous positive airway pressure (CPAP) treatment, the potential role of primary prevention trials targeting sleepy OSA patients, and the use of the pulse wave amplitude drop (PWAD) index as a biomarker for cardiovascular risk in OSA.

This pilot trial aimed to provide evidence for whether the integration of a wearable device with digital behavioral therapy for insomnia (dBTi) improves treatment outcomes and engagement. One hundred and twenty-eight participants with insomnia symptoms were randomized to a 3-week dBTi program (SleepFix®) with a wearable device enabling sleep data synchronization (dBTi+wearable group; n = 62) or dBTi alone (n = 66). Participants completed the Insomnia Severity Index (ISI) and modified Pittsburgh Sleep Quality Index (PSQI) parameters: wake-after-sleep-onset (WASO), sleep-onset-latency (SOL), and total sleep time (TST) at baseline and weeks 1, 2, 3, and primary endpoint of week 6 and follow-up at 12 weeks. Engagement was measured by the number of daily sleep diaries logged in the app. There was no difference in ISI change scores between the groups from pre- to post-treatment (Cohen's d= 0.7, p=.061). The dBTi+wearable group showed greater improvements in WASO (d= 0.8, p =.005) and TST (d= 0.3, p=.049) compared to the dBTi group. Significantly greater engagement (sleep diary entries) was observed in the dBTi+wearable group (mean = 22.4, SD = 10.0) compared to the dBTi group (mean = 14.1, SD = 14.2) (p =.010). This pilot trial found that integration of wearable device with a digital insomnia therapy enhanced user engagement and led to improvements in sleep parameters compared to dBTi alone. These findings suggest that adjunctive wearable technologies may improve digital insomnia therapy effectiveness. [ABSTRACT FROM AUTHOR]