scholarly journals Progesterone Might Be an Active Component of the Sleep-Wake Homeostatic Mechanism

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A550-A550
Author(s):  
Georges Copinschi ◽  
Anne H Caufriez

Abstract Background: Using a randomized, double blind, placebo-controlled, crossover protocol, we have shown previously that progesterone may prevent sleep disturbances but has no action on undisturbed sleep. In that study, 8 healthy postmenopausal women took daily at 2300 h for 3 wk a capsule of either 300 mg of progesterone or placebo. Sleep was polygraphically recorded during the last two nights and, during the second night, blood samples were collected at 15-min intervals using an iv catheter,. During the first night, sleep was normal under placebo and progesterone had no effect. During the second night, blood sampling procedure was associated under placebo with marked sleep disturbances, which were considerably reduced under progesterone: at the group level, mean ± SEM duration of wake after sleep onset (WASO) dropped from 152 ± 37 min to 71 ± 19 min (P = 0.01), and slow-wave sleep (SWS) duration increased from 53 ± 6 min to 79 ± 10 min (P = 0.04). Objective: To submit individual data collected in that study to new analyses designed to further investigate possible mechanism(s) of progesterone actions on sleep architecture. Results: Among individual subjects, no relation could be evidenced between progesterone levels and sleep variables, or between individual progesterone-associated improvements and absolute values of corresponding sleep variables under placebo. By contrast, for WASO and SWS, significant positive correlations (Spearman test) were evidenced between individual responses to progesterone (i.e. the difference, during night 2, between value under progesterone and value under placebo) and corresponding individual alterations caused under placebo by the blood sampling procedure (i.e. the difference, under placebo, between value during night 1 and value during night 2): WASO: rs = 0.74, P = 0.037, n = 8; SWS: rs = 0.86, P = 0.014, n = 7. (Pearson test yielded similar results: WASO: r = 0.85, P = 0.008; SWS: r = 0.76, P = 0.047). Conclusions: Although they obviously need to be confirmed by larger studies performed in a variety of clinical conditions, the present findings suggest that progesterone action on sleep architecture is specifically tailored to restore individual normality rather than group normality. Since SWS is mainly regulated by the sleep-wake homeostatic mechanism relating sleep pressure to the duration of prior wakefulness, it is tempting to speculate that progesterone might be an active component of this mechanism.

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1193-1193
Author(s):  
Anne Caufriez ◽  
Rachel Leproult ◽  
Mireille L'Hermite-Balériaux ◽  
Myriam Kerkhofs ◽  
Georges Copinschi

Abstract Context: A number of neuroactive progesterone metabolites produce sedative-like effects. However, the effects of progesterone administration on sleep are not well characterized. Objective: To investigate the effects of a 3-wk progesterone administration on sleep architecture and multiple hormonal profiles. Subjects: Eight healthy postmenopausal women, 48–74 yr old, without sleep complaints or vasomotor symptoms. None was on hormone replacement therapy. They did not take any medication for ≥2 months. Design: Randomized, double-blind, placebo-controlled study. For 3 wk, subjects took daily at 2300 h a capsule of either 300 mg of progesterone or placebo. Sleep was polygraphically recorded during the last two nights, and blood samples were obtained at 15-min intervals for 24 h. Results: During the first night (no blood sampling), sleep was similar in both conditions. Under placebo, blood sampling procedure was associated with marked sleep disturbances, which were considerably reduced under progesterone treatment: mean duration of wake after sleep onset was 53% lower, slow-wave sleep duration almost 50% higher, and total slow-wave activity (reflecting duration and intensity of deep sleep) almost 45% higher under progesterone than under placebo (P ≤ 0.05). Nocturnal GH secretion was increased, and evening and nocturnal TSH levels were decreased under progesterone (P ≤ 0.05). Conclusions: Progesterone had no effect on undisturbed sleep but restored normal sleep when sleep was disturbed (while currently available hypnotics tend to inhibit deep sleep), acting as a “physiologic” regulator rather than as a hypnotic drug. Use of progesterone might provide novel therapeutic strategies for the treatment of sleep disturbances, in particular in aging where sleep is fragmented and of lower quality.


Author(s):  
Ganesh Ingole ◽  
Harpreet S. Dhillon ◽  
Bhupendra Yadav

Background: A prospective cohort study to correlate perceived sleep disturbances in depressed patients with objective changes in sleep architecture using polysomnography (PSG) before and after antidepressant therapy.Methods: Patients were recruited into the study after applying strict inclusion and exclusion criterion to rule out other comorbidities which could influence sleep. A diagnosis of Depressive episode was made based on ICD-10 DCR. Psychometry, in the form of Beck Depressive inventory (BDI) and HAMD (Hamilton depression rating scale) insomnia subscale was applied on Day 1 of admission. Patients were subjected to sleep study on Day 03 of admission with Polysomnography. Patients were started on antidepressant treatment post Polysomnography. An adequate trial of antidepressants for 08 weeks was administered and BDI score ≤09 was taken as remission. Polysomnography was repeated post remission. Statistical analysis was performed using Kruskal Wallis test and Pearson correlation coefficient.Results: The results showed positive (improvement) polysomnographic findings in terms of total sleep time, sleep efficiency, wake after sleep onset, percentage wake time and these findings were statistically significant. HAM-D Insomnia subscale was found to correlate with total sleep time, sleep efficiency, wake after sleep onset, total wake time and N2 Stage percentage.Conclusions: Antidepressant treatment effectively improves sleep architecture in Depressive disorder and HAM-D Insomnia subscale correlates with objective findings of total sleep time, sleep efficiency, wake after sleep onset, total wake time and duration of N2 stage of NREM.


Author(s):  
Mohamed A. Tork ◽  
Hebatallah R. Rashed ◽  
Lobna Elnabil ◽  
Nahed Salah-Eldin ◽  
Naglaa Elkhayat ◽  
...  

Abstract Background Sleep disorders and epilepsy commonly exist and affect each other. Patients with epilepsy often complain of poor sleep and on the other hand, poor sleep makes epilepsy control difficult. Objectives We aimed at comparing the sleep disturbances in a group of patients with medically controlled epilepsy versus another group with medically refractory epilepsy, from the electrophysiological standpoint. Subjects and methods Sixty epilepsy patients were included; half of them with controlled epilepsy were assigned as group I, and the other half with refractory epilepsy was assigned as group II. All patients had an overnight polysomnogram and sleep EEG done. We excluded any patient with abnormal general or neurological clinical examination. Results Patients in group II, had significantly delayed sleep onset latency and REM latency. However, higher arousal index, insomnia, and periodic limb movement index were found to be significantly higher in group I. Respiratory events; as light sleep durations, were observed to be higher in Group II, in addition to apnea-hypopnea index that was significantly higher in this group. Conclusion Epilepsy affects sleep architecture and sleep-related events. Patients with refractory epilepsy suffer from more disturbance in sleep patterns. Moreover, antiepileptic drugs can have a diverse effect on sleep architecture and quality in epileptic patients.


2017 ◽  
Vol 117 (7) ◽  
pp. 979-984 ◽  
Author(s):  
Insung Park ◽  
Ryuji Ochiai ◽  
Hitomi Ogata ◽  
Momoko Kayaba ◽  
Sayaka Hari ◽  
...  

AbstractChlorogenic acids (CGA) are the most abundant polyphenols in coffee. Continuous consumption of CGA reduces body fat and body weight. Since energy metabolism and sleep are controlled by common regulatory factors, consumption of CGA might modulate sleep. Lack of sleep has been identified as a risk factor for obesity, hypertension and type 2 diabetes. The aim of this study was to determine the effects of ingesting CGA over 5 d on energy metabolism and sleep quality in humans. A total of nine healthy subjects (four male and five female) completed a placebo-controlled, double-blinded, cross-over intervention study. Subjects consumed a test beverage containing 0 or 600 mg of CGA for 5 d. On the fifth night, subjects stayed in a whole-room metabolic chamber to measure energy metabolism; sleep was evaluated using polysomnographic recording. It was found that CGA shortened sleep latency (9 (sem 2) v. 16 (sem 4) min, P<0·05) compared with the control, whereas no effect on sleep architecture, such as slow-wave sleep, rapid eye movement or waking after sleep onset, was observed. Indirect calorimetry revealed that consumption of CGA increased fat oxidation (510 (sem 84) kJ/8 h (122 (sem 20) kcal/8 h) v. 331 (sem 79) kJ/8 h (81 (sem 19) kcal/8 h), P<0·05) but did not affect energy expenditure during sleep. Consumption of CGA enhanced parasympathetic activity assessed from heart-rate variability during sleep (999 (sem 77) v. 919 (sem 54), P<0·05). A period of 5-d CGA consumption significantly increased fat oxidation during sleep, suggesting that beverages containing CGA may be beneficial to reduce body fat and prevent obesity. Consumption of CGA shortened sleep latency and did not adversely affect sleep quality.


1996 ◽  
Vol 270 (4) ◽  
pp. E608-E613 ◽  
Author(s):  
L. Weibel ◽  
K. Spiegel ◽  
M. Follenius ◽  
J. Ehrhart ◽  
G. Brandenberger

To determine whether the circadian system of night workers is adapted to a night-active schedule, we submitted 11 night workers and 11 day-active subjects to a 10-min blood sampling procedure during their usual sleep-wake cycle, permitting a precise determination of circadian and ultradian cortisol variations. In night works, the usual shift of 8 h in the sleep period was associated with a distortion of the normal 24-h cortisol rhythm. The acrophase exhibited a shift of approximately 6.5 h, whereas the quiescent period, abruptly interrupted by a large peak, underwent a shift of only 3 h and lasted for approximately 5 h, as in day-active subjects. Slow-wave sleep and sleep onset occurred during periods of low or decreasing cortisol secretory rates, whereas awakenings were associated with an increase in cortisol secretory rates. These results revealed that the circadian system of night workers only partially adapts to night work and that adaptation processes rely on an internal dissociation of the markers of the cortisol pattern, without disturbing the processes that couple cortisol release and specific sleep stages.


Author(s):  
Francisco Freitas ◽  
Mónica Alves

Abstract Background Phlebotomy guidelines discourage tourniquet use whenever possible. We assessed phlebotomists' capability of not using the tourniquet in venous blood sampling, hypothesizing it to be equal to 50% of the patients attended, and identifying the most frequent venipuncture site. Materials and Methods We assigned two phlebotomists of the same age (41 years) and experience (20 years) to record 10 phlebotomy days, the first with prioritized and the latter with nonprioritized patients. Each acquired daily data for the number of attended patients, age, gender, frequency of nontourniquet usage, and punctured vein. To test our work hypothesis we used the two-tailed single sample t-test. Differences between age-group means and nontourniquet use means by each phlebotomist were tested by two-tailed t-test for independent means. Results In 10 phlebotomy days, 683 patients were attended (males 43.2%). We found no statistically significant difference between age-group means. The combined capability of nontourniquet use was 50.5%, which did not differ from our null hypothesis, but the difference in individual group means was statistically significant, the means being 33% and 66.9% (prioritized vs. nonprioritized). The medial cubital vein was the most prone to be punctured (77.7%). Conclusion Performing phlebotomies without tourniquet was possible in at least half of the attended patients, though it was more limited in specific group populations.


2021 ◽  
Vol 13 ◽  
Author(s):  
Gabriel Natan Pires ◽  
Isabela Antunes Ishikura ◽  
Sandra Doria Xavier ◽  
Caetano Petrella ◽  
Ronaldo Delmonte Piovezan ◽  
...  

Since the beginning of the COVID-19 pandemic, older adults have been found to be a highly vulnerable group, with a higher prevalence of severe cases and negative outcomes. Research has focused on the reasons why older adults are at greater risk; Sleep-related factors have been suggested as one possible explanation for this. An individual’s sleep pattern undergoes significant changes over the course of their life. In older adults a specific sleep profile can be observed, one characterized by advanced sleep timing, a morningness preference, longer sleep-onset latency, shorter overall sleep duration, increased sleep fragmentation, reduced slow-wave sleep and, increased wake time after sleep onset. Additionally, an increased prevalence of sleep disorders can be observed, such as obstructive sleep apnea and insomnia. Previous research has already linked sleep disorders (especially sleep apnea) with COVID-19, but few studies have focused specifically on the older population. We believe that the intrinsic sleep patterns of older adults, and the prevalence of sleep disorders in this population, may be important factors that could explain why they are at a greater risk of negative COVID-19 outcomes. In this review, we discuss the relationship between sleep and COVID-19 among older adults, focusing on three different aspects: (1) Sleep-related issues that might increase the likelihood of getting infected by SARS-COV-2; (2) Sleep disturbances that might increase the predisposition to worse COVID-19 prognosis and outcomes; and (3) COVID-19-related aspects affecting community-dwelling older adults, such as social isolation, quarantine, and home confinement, among others, that might impact sleep.


2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Asmaa M. Abumuamar ◽  
Paul Dorian ◽  
David Newman ◽  
Colin M. Shapiro

Introduction. Obstructive sleep apnea (OSA) is common and usually underdetected in patients with cardiac arrhythmia. Ambulatory sleep testing may provide an alternative method for detection of OSA under realistic conditions compared to in-laboratory polysomnography. We aimed to (1) determine the sleep architecture in arrhythmia patients; (2) detect differences in sleep parameters between patients with and without OSA; and (3) compare the results of two consecutive nights of unattended ambulatory sleep testing. Methods. Consecutive patients with unknown OSA status were recruited from arrhythmia clinics. Patients underwent two consecutive nights of self-applied in-home sleep testing replete with electroencephalogram (EEG) recording. Results. One hundred patients were recruited. The mean age was 64±13 years (70% males). OSA (AHI ≥ 5/h) was detected in 85% of patients. In the total sample, the sleep efficiency was reduced, and sleep onset latency was longer compared to a reference population of the same age. In patients with OSA, the sleep efficiency and the percentage of slow wave sleep were reduced; however, the arousal and periodic limb movement indices were increased compared to patients without OSA. The two nights of the ambulatory sleep testing showed consistent results with an excellent test-retest reliability for the AHI (ICC = 0.813). REM latency was shorter during the second night of sleep recording (p=0.02). There were no other significant differences in the sleep architecture, respiratory indices, and other sleep parameters between the first and the second night of the ambulatory sleep recording. Conclusions. There is no significant difference in the respiratory parameters obtained during two consecutive nights of ambulatory sleep testing. Ambulatory studies incorporating EEG may provide a reliable, convenient, and economically efficient method for sleep assessment and there appears to be no significant night-to-night variability.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Ayelet Arazi ◽  
Gal Meiri ◽  
Dor Danan ◽  
Analya Michaelovski ◽  
Hagit Flusser ◽  
...  

Abstract Study Objectives Sleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow-wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD. Methods In this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children. Results Children with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow-wave sleep in comparison to controls. This difference was largest during the first 2 hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents. Conclusions These results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A52-A53
Author(s):  
Larissa Engert ◽  
Marc Dubourdeau ◽  
Rammy Dang ◽  
Janet Mullington ◽  
Monika Haack

Abstract Introduction Sleep disturbances deteriorate immune function by not only affecting pro-inflammatory pathways, but also inflammatory resolution pathways, which actively terminate inflammation. It is assumed that slow wave sleep (SWS) amount and slow wave activity (SWA) convey the immune-supportive functions of sleep. We investigated whether changes in SWS induced by experimental sleep disturbance followed by recovery sleep predict changes in inflammatory resolution mediators. Methods The randomized controlled within-subjects trial (N=24, 20-42 years, 12 women) consisted of two 19-day in-hospital protocols (experimental sleep disturbance/control). After three nights of baseline sleep (8h/night), participants in the experimental sleep disturbance condition were exposed to three cycles of three nights of disturbed sleep (delayed sleep-onset, hourly sleep disruption, advanced sleep-offset) followed by one night of 8h-recovery sleep. The protocol ended with three nights of recovery sleep. In the control condition, participants had uninterrupted sleep (8h/night). Sleep (PSG) and resolvin lipid mediators in plasma (1100h, LC-MS/MS) were assessed at baseline, during the last cycle of sleep disturbance, and during/after the first and third night of final recovery sleep. Data were analyzed using generalized linear mixed models and Pearson/Spearman correlations. Results As expected, SWS amount decreased during experimental sleep disturbance and increased during the first recovery sleep night (p&lt;.001). Similarly, resolvin (Rv) D2 and RvD3 decreased during sleep disturbance and RvD2 increased with subsequent recovery sleep (p&lt;.001). The SWS response did not correlate with the resolvin response to sleep disturbance or to recovery sleep. However, the NREM sleep response correlated with the resolvin response during the third recovery sleep night, i.e., a greater NREM response was associated with a greater RvD2 and RvD3 response (r=.68, p=.002; r=.58, p=.012). In contrast, a greater REM sleep response was associated with a lower resolvin response (r=−.63, p=.005; r=−.66, p=.003). Conclusion These data suggest that during recovery from sleep disturbance, NREM rather than REM sleep promotes inflammatory resolution, thereby acting as the sleep state that protects against low-grade systemic inflammation, which has been frequently observed as a consequence of sleep disturbances. Analysis whether SWA is related to inflammatory resolution is in progress. Support (if any) NIH/NINDS R01-NS091177; NIH/NCRR UL1-RR02758, M01-RR01032; German Research Foundation (DFG) EN1291/1-1.


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