scholarly journals Circadian tau differences and rhythm associations in delayed sleep–wake phase disorder and sighted non-24-hour sleep–wake rhythm disorder

SLEEP ◽  
2020 ◽  
Author(s):  
Gorica Micic ◽  
Nicole Lovato ◽  
Sally A Ferguson ◽  
Helen J Burgess ◽  
Leon Lack
Keyword(s):  
Circadian Rhythm ◽  
Core Body Temperature ◽  
Sleep Onset ◽  
Phase Relationship ◽  
Biological Rhythms ◽  
Circadian Phase ◽  
Behavioral Rhythm ◽  
Rhythm Disorder ◽  
Dim Light ◽  
Delayed Sleep

Abstract Study Objectives We investigated biological and behavioral rhythm period lengths (i.e. taus) of delayed sleep–wake phase disorder (DSWPD) and non-24-hour sleep–wake rhythm disorder (N24SWD). Based on circadian phase timing (temperature and dim light melatonin onset), DSWPD participants were dichotomized into a circadian-delayed and a circadian non-delayed group to investigate etiological differences. Methods Participants with DSWPD (n = 26, 17 m, age: 21.85 ± 4.97 years), full-sighted N24SWD (n = 4, 3 m, age: 25.75 ± 4.99 years) and 18 controls (10 m, age: 23.72 ± 5.10 years) participated in an 80-h modified constant routine. An ultradian protocol of 1-h “days” in dim light, controlled conditions alternated 20-min sleep/dark periods with 40-min enforced wakefulness/light. Subjective sleepiness ratings were recorded prior to every sleep/dark opportunity and median reaction time (vigilance) was measured hourly. Obtained sleep (sleep propensity) was derived from 20-min sleep/dark opportunities to quantify hourly objective sleepiness. Hourly core body temperature was recorded, and salivary melatonin assayed to measure endogenous circadian rhythms. Rhythm data were curved using the two-component cosine model. Results Patients with DSWPD and N24SWD had significantly longer melatonin and temperature taus compared to controls. Circadian non-delayed DSWPD had normally timed temperature and melatonin rhythms but were typically sleeping at relatively late circadian phases compared to those with circadian-delayed DSWPD. Conclusions People with DSWPD and N24SWD exhibit significantly longer biological circadian rhythm period lengths compared to controls. Approximately half of those diagnosed with DSWPD do not have abnormally delayed circadian rhythm timings suggesting abnormal phase relationship between biological rhythms and behavioral sleep period or potentially conditioned sleep-onset insomnia.

scholarly journals Whoever Wanted to Catch a Worm, Anyway?

2019 ◽  
pp. 345-363
Author(s):  
Robert Hiensch ◽  
Neomi Shah
Keyword(s):  
Circadian Rhythm ◽  
Young Adulthood ◽  
Sleep Onset ◽  
Strict Adherence ◽  
Sleep Inertia ◽  
Sleep Diaries ◽  
Hygiene Practices ◽  
Rhythm Disorder ◽  
Delayed Sleep ◽  
Circadian Physiology

Delayed sleep/wake phase disorder (DSWPD) is the most common circadian rhythm disorder. It is characterized by persistently delayed sleep onset and wake times relative to conventional norms. Individuals usually present in young adulthood with symptoms of sleep-onset insomnia, sleep inertia, and excessive daytime sleepiness due to sleep deprivation when societal commitments require significantly earlier than desired sleep and wake times. Sleep quality itself is normal. The diagnosis can usually be made by history and sleep diaries. The exact cause of DSWPD is unknown, but genetics, abnormal circadian physiology, and perpetuating behaviors all contribute. Treatment consists of morning phototherapy and evening melatonin at times individualized to the patient’s circadian rhythm. Strict adherence to standard sleep hygiene practices increases the chance of success.

Management of insomnia and circadian rhythm sleep–wake disorders

2020 ◽  
pp. 1167-1178
Author(s):  
Simon D. Kyle ◽  
Alasdair L. Henry ◽  
Colin A. Espie
Keyword(s):  
Circadian Rhythm ◽  
Evidence Based ◽  
Sleep Wake Disorders ◽  
Insomnia Disorder ◽  
Cognitive Behavioural ◽  
Melatonin Administration ◽  
Evidence Based Treatments ◽  
Rhythm Disorder ◽  
Delayed Sleep ◽  
Behavioural Therapies

Insomnia disorder and circadian rhythm sleep–wake disorders (CRSWDs) are prevalent and impairing sleep disorders and often co-present with psychiatric disorder. Insomnia is characterized by difficulty with initiation and/or maintenance of sleep, driven primarily by cognitive behavioural processes. CRSWDs manifest because of alterations to the endogenous circadian clock (intrinsic) or as a consequence of environmental circumstances (extrinsic). This chapter reviews evidence-based treatments for the management of insomnia and intrinsic CRSWDs (delayed sleep–wake phase disorder, advanced sleep–wake phase disorder, non-24-hour sleep–wake disorder, irregular sleep–wake rhythm disorder). The chapter covers cognitive behavioural therapies, sleep-promoting hypnotics, phototherapy, and exogenous melatonin administration. The chapter also highlight gaps in the existing clinical science and reflects on emergent therapeutic approaches.

scholarly journals 0039 The Clinical Utility of Dim Light Melatonin Onset in Treatment of Delayed Sleep-Wake Phase Disorder: Preliminary Findings

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A16-A16
Author(s):  
L Swanson ◽  
J Arnedt ◽  
K DuBuc ◽  
T de Sibour ◽  
H Burgess
Keyword(s):  
Sleep Onset ◽  
Onset Time ◽  
Sleep Diary ◽  
Double Blind ◽  
Exogenous Melatonin ◽  
Research Award ◽  
Dim Light Melatonin Onset ◽  
Wrist Actigraphy ◽  
Dim Light ◽  
Delayed Sleep

Abstract Introduction Delayed sleep-wake phase disorder (DSWPD) is common, debilitating, and challenging to treat. In an ongoing randomized trial, we are comparing exogenous melatonin treatment outcomes in DSWPD participants for whom dim light melatonin onset (DLMO) is measured objectively vs. estimated. Methods Thus far, 13 participants (27±6 years old, 67% female) have completed a randomized, controlled, double-blind 4-week trial of 0.5 mg of exogenous melatonin timed to either 3 h before measured DLMO (M-DLMO, n = 6) or 3 h before DLMO estimated at 2 h before average sleep onset time based on at least 7 days of wrist actigraphy and sleep diary (E-DLMO, n = 7). All participants met International Classification of Sleep Disorders-3 diagnostic criteria for DSWPD and were otherwise healthy. Participants completed 4 weekly treatment sessions with a blinded psychologist; time of melatonin administration and bed-rise schedule were advanced up to 1 h/week. A validated home saliva collection kit measured DLMO in all participants. Between-group t-tests and Hedges’ g effect sizes (ES) were calculated at post-treatment for the following outcomes: DLMO; Pittsburgh Sleep Quality Index (PSQI) global score; Morningness-Eveningness Questionnaire (MEQ); and the actigraphy parameters sleep efficiency (SE) and clock time of sleep onset and offset. A paired-sample t-test compared the measured vs. estimated DLMO at baseline. Results The M-DLMO group had a 65±88 mins DLMO advance vs. 27±30 mins in the E-DLMO group (ES=0.51 p=.381). PSQI scores were similar between groups (M-DLMO=6.67±2.06, E-DLMO=7.1± 1.57, ES=-0.24, p=.646), as were MEQ scores (M-DLMO=43±4.98, E-DLMO=48±12.72, ES=-0.47, p=.387). Sleep onset time (M-DLMO=0:32±1:02, E-DLMO=0:31±1:38, ES=0.01, p=.98) and offset time (M-DLMO=8:05±1:03, E-DLMO=8:08±2:14, ES=-0.02, p=.968) were similar between the groups, although sleep was more efficient in M-DLMO vs. E-DLMO (84%±3% vs. 76%±10%, ES=0.94, p=.096). On average, baseline measured DLMO occurred 123±83 mins earlier than estimated DLMO (p=.001). Conclusion We are continuing to enroll participants in this trial. Preliminary results suggest some potential benefit of measuring the DLMO, but results will need to be clarified in a larger sample. Support American Sleep Medicine Foundation Strategic Research Award

Chronobiological issues of sleep and circadian rhythms

2011 ◽  
Vol 26 (S2) ◽  
pp. 2133-2133
Author(s):  
G. Hajak
Keyword(s):  
Circadian Rhythm ◽  
Clock Genes ◽  
Phase Relationship ◽  
Temporal Organization ◽  
Stable Phase ◽  
Delayed Sleep Phase Syndrome ◽  
Circadian Rhythm Sleep Disorders ◽  
Delayed Sleep Phase ◽  
Circadian Clock Genes ◽  
Delayed Sleep

Progress in unravelling the cellular and molecular basis of mammalian circadian regulation over the past decade has provided us with data that deteriorations in measurable circadian output parameters, such as sleep/wake deficits and dysregulation of circulating hormone levels, are common features of most central nervous system disorders.At the core of the mammalian circadian system is a complex of molecular oscillations within the hypothalamic suprachiasmatic nucleus. These oscillations are modifiable by afferent signals from the environment, and integrated signals are subsequently conveyed to remote central neural circuits where specific output rhythms are regulated. Usually our sleep/wake cycle, temperature and melatonin rhythms are internally synchronized with a stable phase relationship. When there is a desynchrony between the sleep/wake cycle and circadian rhythm, sleep disorders such as advanced and delayed sleep phase syndrome can arise as well as transient chronobiologic disturbances, for example from jet lag and shift work.Increasing evidence suggests that disrupted temporal organization of biological functions impairs behaviour, cognition, affect, and emotion. Furthermore, disruption of circadian clock genes impairs the sleep-wake cycle and social rhythms, which may be implicated in particular in mental disorders. An increasing number of journal publications point to a crucial role of circadian rhythm dysregulations in particular for affective disorders, which should e addressed specifically in modern psychiatry.

scholarly journals The Intersection of Cultural Characteristics and Genetics on the Prevalence of Delayed Sleep Phase Syndrome in Brazilian and Japanese Adults

2020 ◽  
Vol 1 (4) ◽  
pp. 1-6
Author(s):  
Abram Estafanous ◽  
Karim Sedky
Keyword(s):  
Circadian Rhythm ◽  
Environmental Changes ◽  
Clock Genes ◽  
Cultural Characteristics ◽  
Sleep Phase ◽  
Delayed Sleep Phase Syndrome ◽  
Japanese Adults ◽  
Delayed Sleep Phase ◽  
Rhythm Disorder ◽  
Delayed Sleep

Delayed sleep phase syndrome (DSPS) is a circadian rhythm disorder where individuals experience difficulty modifying the time they go to sleep and wake up in response to environmental changes. The circadian rhythm itself is regulated by a variety of clock genes, and various other genes (e.g., AA-NAT gene, CKIϵ gene) code for proteins that regulate clock genes. Various polymorphisms of the clock gene influencers have been shown to increase susceptibility to DSPS. This paper seeks to examine how certain cultural characteristics (e.g., napping, timing of meals, exposure to artificial light) and the presence of the AA-NAT gene (G619A polymorphism) and the CKIϵ gene (S408N polymorphism) influence the prevalence of DSPS amongst Japanese and Brazilian populations.

scholarly journals Effects of Night Illumination on Behavior, Body Mass and Learning in Male Zebra Finches

Birds ◽  
2021 ◽  
Vol 2 (4) ◽  
pp. 381-394
Author(s):  
Abhilash Prabhat ◽  
Mayank Kumar ◽  
Ashwani Kumar ◽  
Vinod Kumar ◽  
Sanjay K. Bhardwaj
Keyword(s):  
Body Mass ◽  
Memory Performance ◽  
Sleep Onset ◽  
Learning Task ◽  
Zebra Finches ◽  
Light At Night ◽  
Sleep Behavior ◽  
Novel Object ◽  
Behavioral Rhythm ◽  
Dim Light

An increase in artificial night lighting has blurred the boundaries of day and night and transformed the natural day-night environment with alteration in the temporal niche of the animals. Male zebra finches were exposed to a dim light at night (dLAN) protocol (Light: dLAN, 12L = 200 lux: 12dLAN = 5 lux) with controls on darkness at night (Light: dark, 12L = 200 lux: 12D = 0 lux) for six weeks. We assayed sleep-wake, daily behaviors, mood, and cognition, as well as changes in physiological parameters. Dim light at night increased sleep frequency, delayed sleep onset, advanced awakening latency, and caused a reduction in total sleep duration. dLAN birds did not associate (physical association) with novel object and birds spent significantly lesser time on perch with novel object as compared to LD. In colour learning task, night illuminated birds took more time to learn and made more error, compared to LD. dLAN significantly altered the 24-h daily behavioral rhythm (amplitude and acrophase) of feeding, drinking, preening, and perch-hopping behavior. In particular, birds extended their feeding hours in the nighttime under dLAN, with no difference in total food intake. Birds under dLAN increased fattening and hence significantly increased body mass. Our results show that dim light at night altered feeding rhythm, caused decrease in sleep behavior, and negatively affected learning and memory performance in male zebra finches.

Late-night presentation of an auditory stimulus phase delays human circadian rhythms

2005 ◽  
Vol 289 (1) ◽  
pp. R209-R216 ◽  
Author(s):  
Namni Goel
Keyword(s):  
Circadian Rhythms ◽  
Auditory Stimulus ◽  
Core Body Temperature ◽  
Biological Clock ◽  
Phase Changes ◽  
Circadian Phase ◽  
Late Night ◽  
Human Circadian Rhythms ◽  
Before And After ◽  
Dim Light

Although light is considered the primary entrainer of circadian rhythms in humans, nonphotic stimuli, including exercise and melatonin also phase shift the biological clock. Furthermore, in birds and nonhuman mammals, auditory stimuli are effective zeitgebers. This study investigated whether a nonphotic auditory stimulus phase shifts human circadian rhythms. Ten subjects (5 men and 5 women, ages 18–72, mean age ± SD, 44.7 ± 21.4 yr) completed two 4-day laboratory sessions in constant dim light (<20 lux). They received two consecutive presentations of either a 2-h auditory or control stimulus from 0100 to 0300 on the second and third nights (presentation order of the stimulus and control was counterbalanced). Core body temperature (CBT) was collected and stored in 2-min bins throughout the study and salivary melatonin was obtained every 30 min from 1900 to 2330 on the baseline and poststimulus/postcontrol nights. Circadian phase of dim light melatonin onset (DLMO) and of CBT minimum, before and after auditory or control presentation was assessed. The auditory stimulus produced significantly larger phase delays of the circadian melatonin (mean ± SD, −0.89 ± 0.40 h vs. −0.27 ± 0.16 h) and CBT (−1.16 ± 0.69 h vs. −0.44 ± 0.27 h) rhythms than the control. Phase changes for the two circadian rhythms also positively correlated, indicating direct effects on the biological clock. In addition, the auditory stimulus significantly decreased fatigue compared with the control. This study is the first demonstration of an auditory stimulus phase-shifting circadian rhythms in humans, with shifts similar in size and direction to those of other nonphotic stimuli presented during the early subjective night. This novel stimulus may be a useful countermeasure to facilitate circadian adaptation after transmeridian travel or shift work.

scholarly journals Relationship of Morning Cortisol to Circadian Phase and Rising Time in Young Adults with Delayed Sleep Times

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Mark S. Rea ◽  
Mariana G. Figueiro ◽  
Katherine M. Sharkey ◽  
Mary A. Carskadon
Keyword(s):  
Experimental Data ◽  
Secondary Analysis ◽  
Cortisol Awakening Response ◽  
Circadian Phase ◽  
Morning Cortisol ◽  
Dim Light ◽  
Delayed Sleep ◽  
Relationship Of ◽  
The Relationship ◽  
Rising Time

The present study was aimed at further elucidating the relationship between circadian phase, rising time, and the morning cortisol awakening response (CAR). The results presented here are a secondary analysis of experimental data obtained from a study of advanced sleep-wake schedules and light exposures on circadian phase advances measured by dim-light melatonin onset (DLMO). The present results demonstrate that morning CAR is strongly related to rising time and more weakly related to DLMO phase.

scholarly journals 0006 The Role of Stress in Sleep in Night Shift Workers: Going Beyond Circadian Misalignment

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A2-A3
Author(s):  
E Schaap ◽  
C Sagong ◽  
A S Cuamatzi Castelan ◽  
J Sayed ◽  
T Roth ◽  
...  
Keyword(s):  
Sleep Disturbance ◽  
Sleep Duration ◽  
Shift Work ◽  
Night Shift ◽  
Sleep Onset ◽  
Shift Workers ◽  
Circadian Misalignment ◽  
Circadian Phase ◽  
Falling Asleep ◽  
Dim Light

Abstract Introduction Despite a growing need for nighttime work, few studies have characterized the causes of sleep disturbance in night shift workers beyond circadian misalignment. Recent research suggest that high sleep reactivity to stress (a predisposition for sleep disturbance due to stress) may also lead to sleep difficulties in shift workers. This study investigated if sleep reactivity is an independent predictor of daytime sleep disturbances after controlling for circadian phase. Methods Night shift workers (N= 48) completed an 8 hour polysomnography (PSG) during the daytime following a night shift (9am - 4pm). Circadian phase was measured using melatonin assays of saliva samples collected over 24 hours under dim light (&lt;10 lux; Dim Light Melatonin Onset [DLMO]). Sleep reactivity was measured using the Ford Insomnia Response to Stress Test (FIRST). Linear regressions were conducted with PSG sleep parameters as outcome variables: difficulty falling asleep (Sleep Onset Latency [SOL] and Latency to Persistent Sleep [LPS]), difficulty staying asleep (Wake After Sleep Onset [WASO]), and sleep duration (Total Sleep Time [TST]). FIRST was tested as a predictor controlling for DLMO. Results After controlling for circadian phase, higher FIRST scores was associated with more difficulty staying asleep (WASO: t[45]=4.059, p&lt;0.001) and shorter sleep duration (TST: t[45] = -4.403, p&lt;0.0001), but not predictive of difficulty falling asleep (SOL: p&gt;0.05). However, higher FIRST scores did predict a longer latency to persistent sleep (LPS: t[45]=2.272, p&lt;0.05). Conclusion These results suggest that sleep reactivity to stress and circadian misalignment are independent processes that are both associated with disrupted daytime sleep in night shift workers. Given that night shift work can also cause psychosocial stress, treatments focused on circadian misalignment alone may not be sufficient. Our study highlights the need to consider sleep reactivity in the clinical management of shift work disorder. Support Support for this study was provided to PC by NHLBI (K23HL138166).

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