Journal of affective disorders · 2011
Delayed sleep phase syndrome is related to seasonal affective disorder.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Lee Heon-Jeong, Rex Katharine M, Nievergelt Caroline M, Kelsoe John R, Kripke Daniel F
Аннотация
BACKGROUND: Both delayed sleep phase syndrome (DSPS) and seasonal affective disorder (SAD) may manifest similar delayed circadian phase problems. However, the relationships and co-morbidity between the two conditions have not been fully studied. The authors examined the comorbidity between DSPS and SAD.
METHODS: We recruited a case series of 327 DSPS and 331 controls with normal sleep, roughly matched for age, gender, and ancestry. Both DSPS and controls completed extensive questionnaires about sleep, the morningness-eveningness trait, depression, mania, seasonality of symptoms, etc.
RESULTS: The prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ(2)=12.65, p=0.002). DSPS were 3.3 times more likely to report SAD (odds ratio, 3.34; 95% CI, 1.41-7.93) compared to controls as defined by the Seasonal Pattern Assessment Questionnaire (SPAQ). Correspondingly, DSPS showed significantly higher seasonality scores compared to controls in mood, appetite, and energy level subscores and the global seasonality score (t=3.12, t=0.002; t=2.04, p=0.041; t=2.64, p=0.008; and t=2.15, p=0.032, respectively). Weight fluctuation during seasons and winter-summer sleep length differences were also significantly higher in DSPS than controls (t=5.16, p<0.001 and t=2.64, p=0.009, respectively). SAD and S-SAD reported significantly higher eveningness, higher depression self-ratings, and more previous mania symptoms compared to non-seasonal subjects regardless of whether they were DSPS or controls.
CONCLUSIONS: These cases suggested that DSPS is partially comorbid with SAD. These data support the hypothesis that DSPS and SAD may share a pathophysiological mechanism causing delayed circadian phase.
METHODS: We recruited a case series of 327 DSPS and 331 controls with normal sleep, roughly matched for age, gender, and ancestry. Both DSPS and controls completed extensive questionnaires about sleep, the morningness-eveningness trait, depression, mania, seasonality of symptoms, etc.
RESULTS: The prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ(2)=12.65, p=0.002). DSPS were 3.3 times more likely to report SAD (odds ratio, 3.34; 95% CI, 1.41-7.93) compared to controls as defined by the Seasonal Pattern Assessment Questionnaire (SPAQ). Correspondingly, DSPS showed significantly higher seasonality scores compared to controls in mood, appetite, and energy level subscores and the global seasonality score (t=3.12, t=0.002; t=2.04, p=0.041; t=2.64, p=0.008; and t=2.15, p=0.032, respectively). Weight fluctuation during seasons and winter-summer sleep length differences were also significantly higher in DSPS than controls (t=5.16, p<0.001 and t=2.64, p=0.009, respectively). SAD and S-SAD reported significantly higher eveningness, higher depression self-ratings, and more previous mania symptoms compared to non-seasonal subjects regardless of whether they were DSPS or controls.
CONCLUSIONS: These cases suggested that DSPS is partially comorbid with SAD. These data support the hypothesis that DSPS and SAD may share a pathophysiological mechanism causing delayed circadian phase.