Brief reportDelayed sleep phase in young people with unipolar or bipolar affective disorders
Introduction
The internal relationship between the 24-h sleep–wake cycle and endogenous circadian rhythmicity is a major determinant of mood (Boivin et al., 1997, Dijk and Lockley, 2002). Circadian disturbances may play a key role in the pathogenesis of some affective disorders (Borbely and Wirz-Justice, 1982, Germain and Kupfer, 2008). As new therapeutic tools target the circadian system (Hickie and Rogers, 2011, Kupfer et al., 2011, Wirz-Justice et al., 2009), a better understanding of the specific relationship between circadian dysfunction and affective disorders is needed.
The timing of the circadian clock is disturbed in some patients with affective disorders. While early models associated depression with a circadian phase advance (Wehr et al., 1979), other studies suggest phase delay (Hasler et al., 2010, Kitamura et al., 2010), or similar rates of phase advance and delay (Tsujimoto et al., 1990). Importantly, higher levels of ‘eveningness’ in patients with unipolar or bipolar depression are associated with younger age (Drennan et al., 1991). Although circadian phase delay is characteristic of the adolescent developmental period (Crowley et al., 2007), it is unclear whether it is exacerbated in young people with affective disorders. A recent actigraphy study found no significant difference in sleep onset/offset times between adolescents with bipolar disorders and controls, but this was based on only four recording nights (Mullin et al., 2011).
There is a growing interest on the health of ‘young people’ (i.e. 10–24 years old as defined by the Wold Health Organisation) to inform early treatment strategies (Gore et al., 2011, Sawyer et al., 2012). This study investigates objectively the 24-h sleep–wake cycle in adolescents and young adults with mood disorders.
Section snippets
Participants
Seventy-five young help-seeking persons with mood disorders (aged between 13 and 35 years, 62.7% females) were recruited from specialised assessment and early intervention services for mental health problems in young people [Youth Mental Health Clinic at the Brain & Mind Research Institute; and headspace, Campbelltown, Sydney, Australia (Scott et al., 2009, Scott et al., 2012)]. Twenty healthy controls from the same age group also participated in this study (60.0% females). Participants from
Results
Fig. 1 presents the distribution of SON/OFF in each group. The proportion of individuals with delayed sleep phase in the bipolar group was significantly higher than that in the unipolar group (62.1% and 30.4% respectively, corrected χ2=6.0, p=0.014) and control group (10.0%, corrected χ2=11.2, p<0.001). There was no significant difference in the proportion of individuals with delayed sleep phase in the unipolar and control groups (corrected χ2=2.2, p=0.142). A similar sleep phase delay
Discussion
Using objective measures of sleep–wake behaviour, this study demonstrates that the sleep phase of young persons with mood disorders in a depressed phase is delayed, and that this effect is more pronounced in those with bipolar disorders than in those with unipolar depression. Patients with unipolar depression and those with bipolar disorders had a similar level of sleep fragmentation. Thus, while poor sleep may be seen as a hallmark of major depression, sleep phase delay may be more strongly
Role of funding source
EMS and IBH have received educational and research programs/grants that are supported by the pharmaceutical industry (including Servier, Pfizer, AstraZeneca, and Eli Lilly).
Conflict of interest
No conflict declared.
Acknowledgements
The authors would like to express their gratitude to individuals that participated in this study.
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