Longitudinal observations call into question the scientific consensus that humans are unaffected by lunar cycles.

Recent longitudinal observations show that human menstrual cycles, sleep-wake cycles and manic-depressive cycles can become synchronized with lunar cycles, but do so in uniquely complex and heterogeneous ways that are unlikely to have been detected by past studies. Past studies' negative results have given rise to a scientific consensus that human biology and behavior are unaffected by lunar cycles. The recent observations show that synchrony can be temporary, and can occur with more than one type of lunar cycle, more than one phase of a lunar cycle and more than one resonant frequency of a lunar cycle. Given the variability of human responses to lunar cycles, aggregate analyses used in almost all previous studies would likely have cancelled out individuals' responses and led to false negative results. In light of these observations, the question of lunar influence should be investigated further, with longitudinal observations and case-by-case analyses of individuals' data.

Can People Sleep Too Much? Effects of Extended Sleep Opportunity on Sleep Duration and Timing.

Many people are concerned about whether they are getting "enough" sleep, and if they can "sleep too much." These concerns can be approached scientifically using experiments probing long-term (i.e., multi-night) sleep homeostatic processes, since homeostatic processes move the system toward its physiological setpoint (i.e., between "not enough" and "too much"). We analyzed sleep data from two human studies with sleep opportunities much longer than people usually stay in bed (i.e., conditions in which sleep homeostatic responses could be documented): sleep opportunities were 14-16 h per day for 3-28 days. Across the nights of the extended sleep opportunities, total sleep duration, Rapid Eye Movement (REM) sleep duration and non-REM sleep durations decreased and sleep latency increased. Multiple nights were required to reach approximately steady-state values. These results suggest a multi-day homeostatic sleep process responding to self-selected insufficient sleep duration prior to the study. Once steady state-values were reached, there were large night-to-night variations in total sleep time and other sleep metrics. Our results therefore answer these concerns about sleep amount and are important for understanding the basic physiology of sleep and for two sleep-related topics: (i) the inter-individual and intra-individual variability are relevant to understanding "normal" sleep patterns and for people with insomnia and (ii) the multiple nights of sleep required for recovery from insufficient sleep from self-selected sleep loss is important for public health and other efforts for reducing the adverse effects of sleep loss on multiple areas of physiology.

Synchrony Between Bipolar Mood Cycles and Lunar Tidal Cycles Ended After Initiation of Light Treatment and Treatment of Hypothyroidism.

According to a recent report, mood cycles in a group of patients with rapid cycling bipolar disorder oscillated in synchrony with lunar gravimetric tides. Mood switches in a 67-year-old woman with rapid cycling bipolar II disorder on lithium maintenance treatment were assessed with a χ periodogram and a χ analysis of the mood switches in relation to the lunar tidal cycle. During a period when she was treated with nortriptyline and her thyroid-stimulating hormone levels were elevated, her mood switches had a significant (P<0.05) 29- to 30-day periodicity, and the χ analysis showed that the switches were distributed nonrandomly in relation to the spring-neap lunar tidal cycle (P<0.0001); 14 of 15 switches occurred within 2 days of the spring tides. After nortriptyline was discontinued, thyroid-stimulating hormone levels were normalized with treatment with levothyroxine, and consistent bright light treatment was started, the synchrony between mood cycles and lunar cycles disappeared, and rapid cycling eventually stopped. The possibility that lunar mood cycling is sometimes contingent on antidepressant treatment, decreased thyroid function, and certain types of light-dark cycles needs to be considered in future research on lunar tidal influences on the course of bipolar illness.

Bipolar mood cycles associated with lunar entrainment of a circadian rhythm.

In bipolar disorder, episodes of depression and mania are associated with dramatic disturbances in sleep, which experiments show are likely to contribute to the pathogenesis of the episodes. A recent finding that 18 patients' manic-depressive cycles oscillated in synchrony with biweekly surges in amplitude of the moon's tides provided a clue to the cause of the sleep-disturbances. Analyses of one of the patients' sleep-wake cycles suggest that his mood cycles arose when a circadian rhythm that normally is entrained to dawn and controls the daily onset of wakefulness became entrained instead to 24.8-h recurrences of every second 12.4-h tidal cycle. The finding provides the basis for a comprehensive description of the pathogenesis and pathophysiology of the mood cycle.

A longer biological night in long sleepers than in short sleepers.

Habitual sleep duration varies greatly among individuals. The physiological basis of this variation is unknown. We sought to determine whether individual differences in sleep duration are associated with systematic differences in the duration of the biological night that is programmed by the circadian pacemaker and reflected in the nocturnal interval of circadian rhythms in neuroendocrine function, body temperature, and arousal. Ten young, healthy long sleepers (sleep duration >9 h) and 14 short sleepers (<6 h) were studied under constant environmental conditions and in the absence of sleep. The nocturnal intervals of high plasma melatonin levels, increasing cortisol levels, low body temperature, and increasing sleepiness were longer in long sleepers than in short sleepers. The maxima in cortisol and sleepiness exhibited a close relationship to habitual wake-up time, which occurred approximately 2.5 h later in long sleepers than in short sleepers. It is concluded that the circadian pacemaker programs a longer biological night in long sleepers than in short sleepers. We propose that individual differences in the circadian pacemaker's program may contribute to the variability of sleep duration in the general population. The persistence or inertia of an individual's circadian program, as was evident in constant conditions, may underlie the commonly experienced difficulty of changing habitual sleep duration willfully.

Patients with seasonal affective disorder have lower odor detection thresholds than control subjects.

BACKGROUND: Behavioral changes in patients with seasonal affective disorder resemble seasonal changes in photoperiodic animals. Because the olfactory system has a modulatory role in seasonal photoperiodic responses in certain species, we hypothesized that olfactory function may differ between patients with seasonal affective disorder and healthy control subjects. METHODS: Fourteen patients who had winter seasonal affective disorder and 16 healthy volunteers were studied once in winter and once in the subsequent summer. We administered a phenyl ethyl alcohol detection threshold test to each side of the nose in a counterbalanced order, with the nostril contralateral to the tested site occluded. Patient and control data were compared using a 4-way repeated measure analysis of covariance (with group and gender as between-subjects factors, season and side-of-the-nose as within-subjects factors, and age as a covariate). RESULTS: The patients exhibited lower thresholds than did the controls (F(1,25) = 9.2; P =.006). There was no main effect of season. CONCLUSION: In humans, marked seasonal behavioral rhythms with recurrent winter depression may be associated with a more acute sense of smell.

Spontaneous sleep interruptions during extended nights. Relationships with NREM and REM sleep phases and effects on REM sleep regulation.

OBJECTIVES: There is no agreement in the literature as to whether sleep interruption causes rapid eye movement (REM) pressure to increase, and if so, whether this increase is expressed as shortened REM latency, increased REM density, or increased duration of REM sleep. The purpose of the present study was to examine the effect of different durations of spontaneous sleep interruptions on the regulation of REM sleep that occurs after return to sleep. METHODS: The occurrence of spontaneous periods of wakefulness and their effects on subsequent REM sleep periods were analysed in a total sample of 1189 sleep interruptions which occurred across 364 extended nights in 13 normal subjects. RESULTS: Compared with sleep interruptions that last less than 10 min, sleep interruptions that last longer than 10 min occur preferentially out of REM sleep. In both the short and long types of sleep interruptions, the duration of REM periods that ended in wakefulness were shorter than the duration of those that were not interrupted by wakefulness. REM densities of the REM periods that terminated in periods of wakefulness were higher than those of uninterrupted REM periods. The proportion of episodes of wakefulness following REM sleep that were long-lasting progressively increased over the course of the extended night period. The sleep episodes that followed the periods of wakefulness were characterised by a short REM latency. REM duration was increased in episodes that followed long sleep interruptions compared to those that followed short sleep interruptions. REM density did not appear to change significantly in the episodes that followed sleep interruption. CONCLUSIONS: REM sleep mechanisms appear to be the main force controlling sleep after a spontaneous sleep interruption, presumably because during the second half of the night, where more sleep interruptions occur, the pressure for non-rapid eye movement sleep is reduced and the circadian rhythm in REM sleep propensity reaches its peak. Processes promoting REM sleep at the end of the night are consistent with the Pittendrigh and Daan dual oscillator model of the circadian pacemaker.