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Consistent sleep onset and maintenance of body weight after weight loss: An analysis of data from the NoHoW trial.
Larsen, SC, Horgan, G, Mikkelsen, MK, Palmeira, AL, Scott, S, Duarte, C, Santos, I, Encantado, J, O'Driscoll, R, Turicchi, J, et al
PLoS medicine. 2020;(7):e1003168
Abstract
BACKGROUND Several studies have suggested that reduced sleep duration and quality are associated with an increased risk of obesity and related metabolic disorders, but the role of sleep in long-term weight loss maintenance (WLM) has not been thoroughly explored using prospective data. METHODS AND FINDINGS The present study is an ancillary study based on data collected on participants from the Navigating to a Healthy Weight (NoHoW) trial, for which the aim was to test the efficacy of an evidence-based digital toolkit, targeting self-regulation, motivation, and emotion regulation, on WLM among 1,627 British, Danish, and Portuguese adults. Before enrolment, participants had achieved a weight loss of ≥5% and had a BMI of ≥25 kg/m2 prior to losing weight. Participants were enrolled between March 2017 and March 2018 and followed during the subsequent 12-month period for change in weight (primary trial outcome), body composition, metabolic markers, diet, physical activity, sleep, and psychological mediators/moderators of WLM (secondary trial outcomes). For the present study, a total of 967 NoHoW participants were included, of which 69.6% were women, the mean age was 45.8 years (SD 11.5), the mean baseline BMI was 29.5 kg/m2 (SD 5.1), and the mean weight loss prior to baseline assessments was 11.4 kg (SD 6.4). Objectively measured sleep was collected using the Fitbit Charge 2 (FC2), from which sleep duration, sleep duration variability, sleep onset, and sleep onset variability were assessed across 14 days close to baseline examinations. The primary outcomes were 12-month changes in body weight (BW) and body fat percentage (BF%). The secondary outcomes were 12-month changes in obesity-related metabolic markers (blood pressure, low- and high-density lipoproteins [LDL and HDL], triglycerides [TGs], and glycated haemoglobin [HbA1c]). Analysis of covariance and multivariate linear regressions were conducted with sleep-related variables as explanatory and subsequent changes in BW, BF%, and metabolic markers as response variables. We found no evidence that sleep duration, sleep duration variability, or sleep onset were associated with 12-month weight regain or change in BF%. A higher between-day variability in sleep onset, assessed using the standard deviation across all nights recorded, was associated with weight regain (0.55 kg per hour [95% CI 0.10 to 0.99]; P = 0.016) and an increase in BF% (0.41% per hour [95% CI 0.04 to 0.78]; P = 0.031). Analyses of the secondary outcomes showed that a higher between-day variability in sleep duration was associated with an increase in HbA1c (0.02% per hour [95% CI 0.00 to 0.05]; P = 0.045). Participants with a sleep onset between 19:00 and 22:00 had the greatest reduction in diastolic blood pressure (DBP) (P = 0.02) but also the most pronounced increase in TGs (P = 0.03). The main limitation of this study is the observational design. Hence, the observed associations do not necessarily reflect causal effects. CONCLUSION Our results suggest that maintaining a consistent sleep onset is associated with improved WLM and body composition. Sleep onset and variability in sleep duration may be associated with subsequent change in different obesity-related metabolic markers, but due to multiple-testing, the secondary exploratory outcomes should be interpreted cautiously. TRIAL REGISTRATION The trial was registered with the ISRCTN registry (ISRCTN88405328).
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SLEep among diabetic patients and their GlycaEmic control (SLEDGE): A pilot observational study.
Raj, JP, Hansdak, SG, Naik, D, Mahendri, NV, Thomas, N
Journal of diabetes. 2019;(2):122-128
Abstract
BACKGROUND Recent cohort studies have proven the association between sleep deprivation and adverse glycemic control (GC). The aim of this study was to assess the prevalence of excessive daytime sleepiness (EDS), a subjective measure of sleep deprivation, among type 2 diabetic mellitus (T2DM) patients and its association with GC. METHODS This cross-sectional study was conducted between July 2015 and June 2016 in five diabetes clinics in the district of Erode, Tamil Nadu, India. An equal number of consenting patients with T2DM was recruited consecutively from each of the centers, and EDS was measured subjectively using the Epworth sleepiness scale (ESS), whereas GC was assessed using HbA1c levels. RESULTS In all, 126 patients were screened and 102 were found eligible for the study. The prevalence of EDS was 17.5% (95% confidence interval 10.13-24.87). The association between ESS scores and HbA1c levels was analyzed using linear regression after adjusting for age, dietary intake, inflammatory markers (erythrocyte sedimentation rate), depression (Patient Health Questionnaire-9 score) and stress (Perceived Stress Scale score): for every unit increase in the ESS score, HbA1c increased by 0.143 g/dL (P < 0.001). CONCLUSION Subjective EDS was seen in approximately one-quarter of patients with diabetes in our population. There was a positive association between EDS and glycemic control. Screening of patients with diabetes for EDS should be part of routine diabetes management.
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Polysomnographic Findings in Fragile X Syndrome Children with EEG Abnormalities.
Carotenuto, M, Roccella, M, Pisani, F, Matricardi, S, Verrotti, A, Farello, G, Operto, FF, Bitetti, I, Precenzano, F, Messina, G, et al
Behavioural neurology. 2019;:5202808
Abstract
Fragile X syndrome (FXS) is a genetic syndrome with intellectual disability due to the loss of expression of the FMR1 gene located on chromosome X (Xq27.3). This mutation can suppress the fragile X mental retardation protein (FMRP) with an impact on synaptic functioning and neuronal plasticity. Among associated sign and symptoms of this genetic condition, sleep disturbances have been already described, but few polysomnographic reports in pediatric age have been reported. This multicenter case-control study is aimed at assessing the sleep macrostructure and at analyzing the presence of EEG abnormalities in a cohort of FXS children. We enrolled children with FXS and, as controls, children with typical development. All subjects underwent at least 1 overnight polysomnographic recording (PSG). All recorded data obtained from patients and controls were compared. In children with FXS, all PSG-recorded parameters resulted pathological values compared to those obtained from controls, and in FXS children only, we recorded interictal epileptiform discharges (IEDs), as diffuse or focal spikes and sharp waves, usually singles or in brief runs with intermittent or occasional incidence. A possible link between IEDs and alterations in the circadian sleep-wake cycle may suggest a common dysregulation of the balance between inhibitory and excitatory pathways in these patients. The alteration in sleep pattern in children with FXS may negatively impact the neuropsychological and behavioral functioning, adding increasing burn of the disease on the overall management of these patients. In this regard, treating physicians have to early detect sleep disturbances in their patients for tailored management, in order to prevent adjunctive comorbidities.
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Efficacy of melatonin with behavioural sleep-wake scheduling for delayed sleep-wake phase disorder: A double-blind, randomised clinical trial.
Sletten, TL, Magee, M, Murray, JM, Gordon, CJ, Lovato, N, Kennaway, DJ, Gwini, SM, Bartlett, DJ, Lockley, SW, Lack, LC, et al
PLoS medicine. 2018;(6):e1002587
Abstract
BACKGROUND Delayed Sleep-Wake Phase Disorder (DSWPD) is characterised by sleep initiation insomnia when attempting sleep at conventional times and difficulty waking at the required time for daytime commitments. Although there are published therapeutic guidelines for the administration of melatonin for DSWPD, to our knowledge, randomised controlled trials are lacking. This trial tested the efficacy of 0.5 mg melatonin, combined with behavioural sleep-wake scheduling, for improving sleep initiation in clinically diagnosed DSWPD patients with a delayed endogenous melatonin rhythm relative to patient-desired (or -required) bedtime (DBT). METHODS This randomised, placebo-controlled, double-blind clinical trial was conducted in an Australian outpatient DSWPD population. Following 1-wk baseline, clinically diagnosed DSWPD patients with delayed melatonin rhythm relative to DBT (salivary dim light melatonin onset [DLMO] after or within 30 min before DBT) were randomised to 4-wk treatment with 0.5 mg fast-release melatonin or placebo 1 h before DBT for at least 5 consecutive nights per week. All patients received behavioural sleep-wake scheduling, consisting of bedtime scheduled at DBT. The primary outcome was actigraphic sleep onset time. Secondary outcomes were sleep efficiency in the first third of time in bed (SE T1) on treatment nights, subjective sleep-related daytime impairment (Patient Reported Outcomes Measurement Information System [PROMIS]), PROMIS sleep disturbance, measures of daytime sleepiness, clinician-rated change in illness severity, and DLMO time. FINDINGS Between September 13, 2012 and September 1, 2014, 307 participants were registered; 116 were randomised to treatment (intention-to-treat n = 116; n = 62 males; mean age, 29.0 y). Relative to baseline and compared to placebo, sleep onset occurred 34 min earlier (95% confidence interval [CI] -60 to -8) in the melatonin group. SE T1 increased; PROMIS sleep-related impairment, PROMIS sleep disturbance, insomnia severity, and functional disability decreased; and a greater proportion of patients showed more than minimal clinician-rated improvement following melatonin treatment (52.8%) compared to placebo (24.0%) (P < 0.05). The groups did not differ in the number of nights treatment was taken per protocol. Post-treatment DLMO assessed in a subset of patients (n = 43) was not significantly different between groups. Adverse events included light-headedness, daytime sleepiness, and decreased libido, although rates were similar between treatment groups. The clinical benefits or safety of melatonin with long-term treatment were not assessed, and it remains unknown whether the same treatment regime would benefit patients experiencing DSWPD sleep symptomology without a delay in the endogenous melatonin rhythm. CONCLUSIONS In this study, melatonin treatment 1 h prior to DBT combined with behavioural sleep-wake scheduling was efficacious for improving objective and subjective measures of sleep disturbances and sleep-related impairments in DSWPD patients with delayed circadian phase relative to DBT. Improvements were achieved largely through the sleep-promoting effects of melatonin, combined with behavioural sleep-wake scheduling. TRIAL REGISTRATION This trial was registered with the Australian New Zealand Clinical Trials Registry, ACTRN12612000425897.
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Effects of l-Carnosine Supplementation on Sleep Disorders and Disease Severity in Autistic Children: A Randomized, Controlled Clinical Trial.
Mehrazad-Saber, Z, Kheirouri, S, Noorazar, SG
Basic & clinical pharmacology & toxicology. 2018;(1):72-77
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Abstract
Sleep disorders are frequently reported in autistic patients. Evidences suggest that increased oxidative stress and reduced antioxidants may play a major role in the pathogenesis of these disorders. Carnosine acts as an antioxidant, antitoxic and neuroprotective agent. The aim of this trial study was to examine the effects of carnosine supplementation on the sleep disorders and severity of autism core symptoms in autistic patients. In this double-blind, randomized clinical trial, 43 autistic patients (31 boys and 12 girls; aged 4 to 16 years) were divided into two groups of carnosine and control that received 500 mg of carnosine and 500 mg of placebo per day for 2 months, respectively. Sleep disorders were measured using Children's Sleep Habits Questionnaires. Gilliam Autism Rating Scale 2 was used to assess the effects of carnosine supplementation on the autism severity. Carnosine supplementation did not change anthropometric indices (p > 0.05) and showed no effect on autism severity (p > 0.05), whereas it significantly reduced sleep duration (p = 0.04), parasomnias (p = 0.02) and total sleep disorders score by 7.59% (p = 0.006) when compared with the control group. The results suggest that carnosine supplementation could be effective in improving sleep disturbances, in particular sleep duration and parasomnias subscales.
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The effect of a supervised exercise training programme on sleep quality in recently discharged heart failure patients.
Suna, JM, Mudge, A, Stewart, I, Marquart, L, O'Rourke, P, Scott, A
European journal of cardiovascular nursing. 2015;(3):198-205
Abstract
BACKGROUND Sleep disturbances, including insomnia and sleep-disordered breathing, are a common complaint in people with heart failure and impair well-being. Exercise training (ET) improves quality of life in stable heart failure patients. ET also improves sleep quality in healthy older patients, but there are no previous intervention studies in heart failure patients. AIM: The aim of this study was to examine the impact of ET on sleep quality in patients recently discharged from hospital with heart failure. METHODS This was a sub-study of a multisite randomised controlled trial. Participants with a heart failure hospitalisation were randomised within six weeks of discharge to a 12-week disease management programme including exercise advice (n=52) or to the same programme with twice weekly structured ET (n=54). ET consisted of two one-hour supervised aerobic and resistance training sessions, prescribed and advanced by an exercise specialist. The primary outcome was change in Pittsburgh Sleep Quality Index (PSQI) between randomisation and week 12. RESULTS At randomisation, 45% of participants reported poor sleep (PSQI≥5). PSQI global score improved significantly more in the ET group than the control group (-1.5±3.7 vs 0.4±3.8, p=0.03). Improved sleep quality correlated with improved exercise capacity and reduced depressive symptoms, but not with changes in body mass index or resting heart rate. CONCLUSION Twelve weeks of twice-weekly supervised ET improved sleep quality in patients recently discharged from hospital with heart failure.
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Age-related difference in the sleep pressure-lowering effect between an angiotensin II receptor blocker and a calcium channel blocker in Asian hypertensives: the ACS1 Study.
Kario, K, Hoshide, S
Hypertension (Dallas, Tex. : 1979). 2015;(4):729-35
Abstract
Sleep blood pressure (BP), which is partly determined by salt sensitivity and intake, is an important cardiovascular risk in hypertensives. However, there have been no studies on age-related differences in the sleep BP-lowering effect between angiotensin II receptor blockers and calcium channel blockers in Asians. Azilsartan Circadian and Sleep Pressure-the 1st Study was a multicenter, randomized, open-label, 2-parallel-group study conducted to compare the efficacy of 8-week oral treatment with an angiotensin II receptor blocker (azilsartan 20 mg) or a calcium channel blocker (amlodipine 5 mg) on sleep BP as evaluated by ambulatory BP monitoring. Among the overall population, amlodipine treatment achieved significantly greater reduction in sleep BP, awake BP, and 24-hour BP than azilsartan treatment. BP reduction by amlodipine was particularly pronounced in elderly hypertensive patients aged ≥60 years old. Among patients ≥60 years old, the amlodipine group had numerically, but not significantly, higher control rate of sleep BP compared with the azilsartan group. Similar results were found for awake BP and 24-hour BP. These results suggest a greater BP reduction/control by amlodipine compared with azilsartan and that reduction/control of BP by amlodipine was also more effective in the elderly population. As recommended in the American Society of Hypertension/The international Society of Hypertension and the National Institute for Health and Clinical Excellence guidelines for differentiating treatment according to age, amlodipine should be one of the options for starting treatment in the elderly population. CLINICAL TRIAL URL http://clinicaltrials.gov/show/NCT01762501 CLINICAL TRIAL ID NCT01762501.
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Efficacy and tolerability studies evaluating a sleep aid and analgesic combination of naproxen sodium and diphenhydramine in the dental impaction pain model in subjects with induced transient insomnia.
Cooper, S, Laurora, I, Wang, Y, Venkataraman, P, An, R, Roth, T
International journal of clinical practice. 2015;(10):1149-58
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Abstract
STUDY OBJECTIVES The aim of this study was to evaluate the efficacy and tolerability of novel combination naproxen sodium (NS) and diphenhydramine (DPH) in subjects with postoperative dental pain along with transient insomnia induced by 5 h sleep phase advance. The present studies aimed to demonstrate the added benefit and optimal dosages of the combination product over individual ingredients alone in improving sleep and pain. METHODS Each of the two studies was a two-centre, randomised, double-blind and double-dummy trial. In the first study, subjects were randomised into one of the following treatment arms: NS 440 mg/DPH 50 mg, NS 220 mg/DPH 50 mg, NS 440 mg or DPH 50 mg. In the second study, subjects received either NS 440 mg/DPH 25 mg, NS 440 mg or DPH 50 mg. The co-primary end-points in both studies were wake time after sleep onset (WASO) and sleep latency (SL) measured by actigraphy. Other secondary sleep and pain end-points were also assessed. RESULTS The intent-to-treat population included 712 and 267 subjects from studies one and two, respectively. In the first study, only the NS 440 mg/DPH 50 mg combination showed significant improvements in both WASO vs. NS alone (-70.3 min p = 0.0002) and SL vs. DPH alone (25.50 and 41.50 min respectively, p < 0.0001). In the second study, the NS 440 mg/DPH 25 mg combination failed to show any significant improvements vs. either component alone. CONCLUSIONS Only the NS 440 mg/DPH 50 mg combination demonstrated improvement in both sleep latency vs. DPH 50 mg and sleep maintenance (WASO) vs. NS 440 mg. There were no serious or unexpected adverse events reported in either study. CLINICAL TRIAL REGISTRATION NCT01280591 (study 1); NCT01495858 (study 2).
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Sleep architecture following a weight loss intervention in overweight and obese patients with obstructive sleep apnea and type 2 diabetes: relationship to apnea-hypopnea index.
Shechter, A, St-Onge, MP, Kuna, ST, Zammit, G, RoyChoudhury, A, Newman, AB, Millman, RP, Reboussin, DM, Wadden, TA, Jakicic, JM, et al
Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2014;(11):1205-11
Abstract
STUDY OBJECTIVES To determine if weight loss and/ or changes in apnea-hypopnea index (AHI) improve sleep architecture in overweight/ obese adults with type 2 diabetes (T2D) and obstructive sleep apnea (OSA). METHODS This was a randomized controlled trial including 264 overweight/ obese adults with T2D and OSA. Participants were randomized to an intensive lifestyle intervention (ILI) or a diabetes and support education (DSE) control group. Measures included anthropometry, AHI, and sleep at baseline and year-1, year-2, and year-4 follow-ups. RESULTS Changes in sleep duration (total sleep time [TST]), continuity [wake after sleep onset (WASO)], and architecture stage 1, stage 2, slow wave sleep, and REM sleep) from baseline to year 1, 2, and 4 did not differ between ILI and DSE. Repeated-measure mixed-model analyses including data from baseline through year-4 for all participants demonstrated a significant positive association between AHI and stage 1 sleep (p < 0.001), and a significant negative association between AHI and stage 2 (p = 0.01) and REM sleep (p < 0.001), whereas changes in body weight had no relation to any sleep stages or TST. WASO had a significant positive association with change in body weight (p = 0.009). CONCLUSIONS Compared to control, the ILI did not induce significant changes in sleep across the 4-year follow-up. In participants overall, reduced AHI in overweight/ obese adults with T2D and OSA was associated with decreased stage 1, and increased stage 2 and REM sleep. These sleep architecture changes are more strongly related to reductions in AHI than body weight, whereas WASO may be more influenced by weight than AHI. CLINICAL TRIAL REGISTRATION NUMBER NCT00194259.
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Sleep duration and risk of atrial fibrillation (from the Physicians' Health Study).
Khawaja, O, Sarwar, A, Albert, CM, Gaziano, JM, Djoussé, L
The American journal of cardiology. 2013;(4):547-51
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Abstract
Although sleep quality and duration have been related to cardiovascular end points, little is known about the association between sleep duration and incident atrial fibrillation (AF). Hence, we prospectively examined the association between sleep duration and incident AF in a cohort of 18,755 United States male physicians. Self-reported sleep duration was ascertained during a 2002 annual follow-up questionnaire. Incident AF was ascertained through annual follow-up questionnaires. Cox regression analysis was used to estimate the relative risks of AF. The average age at baseline was 67.7 ± 8.6 years. During a mean follow-up of 6.9 ± 2.1 years, 1,468 cases of AF occurred. Using 7 hours of sleep as the reference group, the multivariate adjusted hazard ratio for AF was 1.06 (95% confidence interval 0.92 to 1.22), 1.0 (reference), and 1.13 (95% confidence interval 1.00 to 1.27) from the lowest to greatest category of sleep duration (p for trend = 0.26), respectively. In a secondary analysis, no evidence was seen of effect modification by adiposity (p for interaction = 0.69); however, prevalent sleep apnea modified the relation of sleep duration with AF (p for interaction = 0.01). From the greatest to the lowest category of sleep duration, the multivariate-adjusted hazard ratio for AF was 2.26 (95% confidence interval 1.26 to 4.05), 1.0 (reference), and 1.34 (95% confidence interval 0.73 to 2.46) for those with prevalent sleep apnea and 1.01 (95% confidence interval 0.87 to 1.16), 1.0 (reference), and 1.12 (95% confidence interval 0.99 to 1.27) for those without sleep apnea, respectively. Our data showed a modestly elevated risk of AF with long sleep duration among United States male physicians. Furthermore, a shorter sleep duration was associated with a greater risk of AF in those with prevalent sleep apnea.