In order to clarify the relationship between sleep-wake and core body temperature rhythms in the delayed sleep phase syndrome (DSPS), we conducted simultaneous monitoring of these rhythms in seven patients with DSPS and nine healthy control subjects for 6-10 days during their conventional sleep-wake schedules. The sleep onset and offset times were determined visually from sleep logs, and the temperature data were fitted to 24-hour cosinor curves by the least squares method. The sleep onset and offset times and temperature nadir were delayed significantly in patients with DSPS compared with the control subjects (p = 0.01, 0.003 and 0.02, respectively). We also found that sleep length and the temperature nadir to sleep offset interval were significantly longer in the DSPS than the control group (p = 0.03 and 0.02, respectively). The latter finding suggests that the inability of the patients with DSPS to normally phase-advance their circadian rhythm may be a consequence of masking of the advance portion of their phase-response curve by the last hours of their prolonged sleep episodes.
"Mis - alignment between the biological timing and sleep / wake timing has been proposed as one of the mech - anisms that causes the sleep / wake dysfunction in DSPD . Many studies have documented that sleep / wake timing and circadian markers are delayed in this population relative to healthy controls ( Chang et al . , 2009 ; Ozaki et al . , 1996 ; Shibui et al . , 1999 ; Uchiyama et al . , 2000a"
[Show abstract][Hide abstract] ABSTRACT: Circadian rhythms are near 24-h patterns of physiology and behaviour that are present independent of external cues including hormones, body temperature, mood, and sleep propensity. The term ‘circadian misalignment’ describes a variety of circumstances, such as inappropriately timed sleep and wake, misalignment of sleep/wake with feeding rhythms, or misaligned central and peripheral rhythms. The predominance of early research focused on misalignment of sleep to the biological night. However, discovery of clock genes and the presence of peripheral circadian oscillators have expanded the definitions of misalignment. Experimental studies conducted in animal models and humans have provided evidence of potential mechanisms that link misalignment to negative outcomes. These include dysregulation of feeding behaviours, changes in appetite stimulating hormones, glucose metabolism and mood. This review has two foci: (1) to describe how circadian misalignment has been defined and evaluated in laboratory and field experiments, and (2) to describe evidence linking different types of circadian misalignment to increased risk for physical (cardiovascular disease, diabetes, obesity, cancer) and psychiatric (depression, bipolar, schizophrenia, attention deficit) disorders. This review will describe the role of circadian misalignment as a risk factor for disease in the general population and in clinical populations, including circadian rhythm sleep disorders and psychiatric disorders.
International Review of Psychiatry 06/2014; 26(2). DOI:10.3109/09540261.2014.911149 · 1.80 Impact Factor
"Some believe that the condition represents an extreme manifestation of the delayed circadian preference observed in concert with pubertal development (Carskadon et al., 1997; Carskadon et al., 1993; Jenni et al., 2005). Longer intervals from the core body temperature minimum to sleep offset have been reported among DSPD subjects in comparison to controls, suggesting a contribution from decreased exposure to the phase advance portion of the light phase response curve (PRC) as an etiological factor (Ozaki et al., 1996; Uchiyama et al., 2000; Watanabe et al., 2003). More recent studies (one of which included adolescents (Chang et al., 2009) have not replicated these findings, however (Chang et al., 2009; Mundey et al., 2005; Wyatt et al., 2006). "
[Show abstract][Hide abstract] ABSTRACT: The objective of this study was to compare light exposure and sleep parameters between adolescents with delayed sleep phase disorder (DSPD; n=16, 15.3±1.8 yrs) and unaffected controls (n=22, 13.7±2.4 yrs) using a prospective cohort design. Participants wore wrist actigraphs with photosensors for 14 days. Mean hourly lux levels from 20:00 to 05:00 h and 05:00 to 14:00 h were examined, in addition to the 9-h intervals prior to sleep onset and after sleep offset. Sleep parameters were compared separately, and were also included as covariates within models that analyzed associations with specified light intervals. Additional covariates included group and school night status. Adolescent delayed sleep phase subjects received more evening (p< .02, 22:00-02:00 h) and less morning (p .05, 08:00-09:00 h and 10:00-12:00 h) light than controls, but had less pre-sleep exposure with adjustments for the time of sleep onset (p< .03, 5-7 h prior to onset hour). No differences were identified with respect to the sleep offset interval. Increased total sleep time and later sleep offset times were associated with decreased evening (p< .001 and p= .02, respectively) and morning (p= .01 and p< .001, respectively) light exposure, and later sleep onset times were associated with increased evening exposure (p< .001). Increased total sleep time also correlated with increased exposure during the 9 h before sleep onset (p= .01), and a later sleep onset time corresponded with decreased light exposure during the same interval (p< .001). Outcomes persisted regardless of school night status. In conclusion, light exposure interpretation requires adjustments for sleep timing among adolescents with DSPD. Pre- and post-sleep light exposures do not appear to contribute directly to phase delays. Sensitivity to morning light may be reduced among adolescents with DSPD.
Chronobiology International 12/2011; 28(10):911-20. DOI:10.3109/07420528.2011.619906 · 3.34 Impact Factor
"Ozaki and colleagues  reported a longer interval between body temperature nadir and sleep offset in DSPS patients compared to controls as well as longer sleep episodes , findings since replicated in two studies  . Ozaki and colleagues  suggested that the inability of DSPS patients to phase advance normally might result from not being exposed to the advance portion of their light PRC due to their elongated sleep episodes. Of note is that the interval between body temperature nadir and sleep offset is shorter in normal controls with an evening preference   but longer in DSPS patients, suggesting a discontinuity along the morningness/eveningness dimension. "
[Show abstract][Hide abstract] ABSTRACT: Sleep/wake timing shifts later in young humans during the second decade of life. In this review we describe sleep/wake patterns, changes in these patterns across adolescence, and evidence for the role of environmental, psychosocial, and biological factors underlying these changes. A two-process model incorporating circadian (Process C) and sleep/wake homeostatic (Process S) components is outlined. This model may help us to understand how developmental changes translate to shifted sleep/wake patterns. Delayed sleep phase syndrome (DSPS), which has a typical onset during the second decade of life, may be an extreme manifestation of homeostatic and circadian changes in adolescence. We describe symptoms, prevalence, and possible etiology of DSPS, as well as treatment approaches in adolescents.
Sleep Medicine 10/2007; 8(6):602-12. DOI:10.1016/j.sleep.2006.12.002 · 3.15 Impact Factor
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