Background The folk belief that we should sleep 8 hours seems to be incorrect. Numerous studies have shown that self-reported sleep longer than 7.5 hours or shorter than 6.5 hours predicts increased mortality risk. This study examined if prospectively-determined objective sleep duration, as estimated by wrist actigraphy, was associated with mortality risks. Methods From 1995–1999, women averaging 67.6 years of age provided one-week actigraphic recordings. Survival could be estimated from follow-up continuing until 2009 for 444, with an average of 10.5 years before censoring. Multivariate age-stratified Cox regression models were controlled for history of hypertension, diabetes, myocardial infarction, cancer, and major depression. Results Adjusted survival functions estimated 61% survival (54%–69%, 95% C.I.) for those with sleep less than 300 min and 78% survival (73%–85%, 95% C.I.) for those with actigraphic sleep longer than 390 min, as compared with survival of 90% (85%–94%, 95% C.I.) for those with sleep of 300–390 min. Time-in-bed, sleep efficiency and the timing of melatonin metabolite excretion were also significant mortality risk factors. Conclusion This study confirms a U-shaped relationship between survival and actigraphically measured sleep durations, with the optimal objective sleep duration being shorter than the self-report optimums. People who sleep five or six hours may be reassured. Further studies are needed to identify any modifiable factors for this mortality and possible approaches to prevention.

Measuring different circadian markers suggested different phase relationships between the sleep-wake cycle and endogenous circadian rhythms in aging. Early awakening in older adults cannot be explained simply by a relative phase advance of the circadian system. Evening naps and advanced illumination may play a role in the advance of the circadian system in aging.

Background: The phase of a circadian rhythm reflects where the peak and the trough occur, for example, the peak and trough of performance within the 24 h. Light exposure can shift this phase. More extensive knowledge of the human circadian phase response to light is needed to guide light treatment for shiftworkers, air travelers, and people with circadian rhythm phase disorders. This study tested the hypotheses that older adults have absent or weaker phase-shift responses to light (3000 lux), and that women's responses might differ from those of men.

Background: Delayed sleep phase disorder (DSPD) is a condition in which patients have difficulty falling asleep before the early morning hours and commonly have trouble awakening before late morning or even early afternoon. Several studies have suggested that variations in habitual bedtime are 40-50% heritable.

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, and seasonality of symptoms, etc. Results The prevalences of SAD and subsyndromal SAD (S-SAD) were higher in DSPS compared to controls (χ2=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.