The current study expands upon prior studies of DSPS in 2 important ways: the large sample size in which subjective and objective sleep measures and circadian phase markers were collected and the use of portable data collection of these measures from DSPS patients in their natural home environments. This DSPS population, as a group, demonstrated a consistent delay in the timing of the sleep episode as compared to controls, but based on sleep diaries and wrist actigraphy did not appear to have difficulty falling asleep. Furthermore, they showed no differences in amount of time in bed, sleep duration or sleep efficiency. These results are surprising given that one of the major complaints of DSPS subjects is sleep onset insomnia or an inability to fall asleep at the desired time, which may manifest as long sleep latencies. While there were some DSPS individuals exhibiting particularly long sleep latencies (>1 hour in 8 DSPS and 6 control subjects), the group on average took only 6 minutes longer to fall asleep than controls, a difference that is not significant. This suggests that these DSPS patients were maintaining a habitual sleep schedule that was later than they desired and significantly later than the control group. These patients came to the sleep center to seek treatment to advance the timing of their sleep and wake cycle. Maintaining a delayed bedtime did not appear to show, in our study, adverse consequences of longer sleep latency or decreased sleep efficiency.
A comparison of sleep schedules on weekdays and weekends showed that all participants were going to bed and waking at significantly later times on the weekend. Both DSPS and control groups spent significantly more time in bed and slept longer on weekends, presumably due to a less restricted schedule free from work/school obligations. This indicates that both groups were restricting sleep during weekdays and making up a “sleep deficit” during weekends. It is interesting to note that even though both groups slept significantly more on the weekends, there was no difference between DSPS and control groups in sleep duration for either weekends or weekdays. This result is in contrast to other published reports of DSPS patients having longer sleep durations than control subjects (Ozaki et al., 1996
; Shibui et al., 1999
; Uchiyama et al., 2000
; Watanabe et al., 2003
). Taken together, these results show that the DSPS population studied here had a persistent delay in sleep timing with no evidence for longer sleep duration, difficulty falling asleep or staying asleep. Our findings suggest that under entrained conditions, when allowed to sleep at their habitual sleep times, DSPS patients had normal sleep.
There were significant differences in the circadian phase markers of both temperature and melatonin rhythms with DSPS patients having a characteristically later CBTnadir
and DLMO relative to controls. Examination of the phase relationship between sleep measures and the phase of the body temperature rhythm did not show an alteration between either sleep onset or offset and CBTnadir
in DSPS patients compared with controls. These results differ from reports of a longer phase interval between CBTnadir
and sleep offset in DSPS patients (Ozaki et al., 1996
; Uchiyama et al., 2000
; Watanabe et al., 2003
). In these previous studies, there was no difference in the phase relationship between CBTnadir
and sleep onset, only with sleep offset, which is most likely due to significantly longer sleep durations and therefore later sleep offset times reported in their DSPS patients compared with our population. We found no significant difference in the phase relationship between sleep time and DLMO in DSPS patients compared with controls, as had been previously reported (Shibui et al., 1999
). Again, this may be due to longer sleep durations and subsequent longer interval between wake time and melatonin phase measures in the previously published DSPS group that we did not find in our study. Our findings are consistent with a more recent report (Wyatt et al., 2006
) in which there was no difference in phase angle of DLMO and sleep between DSPS and control groups. Furthermore, it is possible that genetic differences in circadian and homeostatic regulation of sleep and wake may have accounted for the observed difference between the Japanese and US studies, particularly as there have been reported differences in the prevalence of polymorphisms in clock genes reported in different ethnic populations (Ciarleglio et al., 2008
; Hawkins et al., 2008
; Mishima et al., 2005
The significant delay in both phase markers without an accompanying alteration in the phase angle of entrainment suggests that although DSPS subjects exhibit later sleep-wake times under entrained conditions, they are not sleeping at an “adverse” circadian phase for maximum sleep efficiency. This is consistent with our sleep timing results demonstrating that the DSPS group did not show greater sleep latencies than controls. Taken together, our findings suggest that when allowed to sleep at their own habitual schedules, patients with DSPS have both normal sleep parameters and circadian phase angle.
There have been a number of possible explanations proposed for the delayed timing of the sleep episode in DSPS patients, including a longer endogenous circadian period, which would require a greater daily phase advance to entrain to the 24-hour day. If DSPS individuals are not receiving light, the strongest entraining stimulus, at the early part of day where it will cause a phase advance, they may exhibit a delayed sleep schedule. Independent of circadian period length, the sleep-wake schedule for individuals with DSPS, on average, is considerably later than controls and suggests they may not be receiving light in the early portion of the day when they may be still asleep. Furthermore, since they are awake later in the evening/night, they may be receiving light in the delay region of the photic PRC, which would delay their sleep even more. The current study was conducted with individuals living in their home environments, presumably under 24-hour entrained conditions, and therefore endogenous circadian period was not assessed.
Alternatively, it has been proposed that DSPS individuals may have an altered response to light: altered sensitivity to light, smaller phase advance region, or larger phase delay region of the light PRC (Czeisler et al., 1981
). Another possible explanation is that DSPS subjects have an altered phase relationship between their circadian phase and the light/dark cycle. In laboratory studies of young morning- and evening-type individuals, where the light/dark cycle and sleep-wake timing was controlled, there was a phase angle difference showing that morning types were waking at an earlier circadian phase than evening types (Duffy et al., 1999
). While our results do not show an altered phase angle between sleep schedule and circadian phase, we do not know the light/dark conditions, which may differ somewhat from the sleep-wake times for these subjects.
These findings have implications for both diagnosis and treatment of this disorder. At the time of diagnosis of most of the DSPS subjects in this retrospective study, the clinical diagnostic criteria did not require physiologic measures of circadian phase. Since then, there have been revisions made to both the ICSD and DSM-IV criteria that include these measures. Additionally, actigraphy and/or polysomnography have been added to the criteria to confirm the delay of the sleep schedule. Ultimately, the single criterion that remains critical to a clinical diagnosis of DSPS is a self-reported sleep-related complaint by the individual. Results from actigraphic recordings, sleep diaries, and physiologic phase measures, while confirming the delayed timing of the sleep episode and circadian phase, do not support the maladaptive response to this pattern that forms the basis of the sleep complaint. We found no difference in sleep latency, sleep duration, or sleep efficiency between DSPS subjects and controls that would indicate difficulty initiating or maintaining sleep. The analysis of sleep on weekdays and weekends further showed that both groups were extending sleep when given the opportunity, but the DSPS group did not show a longer sleep episode that might indicate greater sleep pressure, relative to the control group. Because we found no significant difference in the phase relationship of sleep timing and circadian phase between the two groups, the DSPS group does not appear to be sleeping at an “adverse” circadian phase that could explain sleep problems. Again, the greater variability seen in the DSPS group suggests that although our measures from the large group, on average, do not differ from the controls, there are likely greater inter-individual differences and multiple symptoms leading to the sleep complaint, suggesting various mechanisms that could explain the consistent delayed sleep phase that is common to these individuals. To this end, objective measures obtained in the subjects’ home environment may be very useful in characterizing a more precise schedule of sleep and timing of circadian phase that may explain the sleep complaint and also help determine the proper manner and timing of treatment.