The endogenous period appears normal.41 A phase delay in process C (as measured by core body temperature or melatonin rhythms in constant routine) has been found,42 but not in all studies or all markers.41,43 The decline in process S (as measured by selleck compound spectral analyses of the sleep electroencephalogram [EEG]) was no different in SAD patients compared with controls.44,45 However, the rise in Inhibitors,research,lifescience,medical process S (as measured by spectral analyses of the wake EEG) was different, indicating a factor related to daytime vigilance.46,47 Wake EEG patterns in evening chronotypes are similar to this,48

which may mean that the above finding is not pathogenetic for SAD, since the patient chronotype is skewed towards ”owls,“ shows the above tendency to phase delay, and has common clock-related polymorphisms.32 War of the zeitgebers? What is fascinating Inhibitors,research,lifescience,medical is that both circadian and wake-dependent factors contribute to a subjective measure such as mood. This has been demonstrated in healthy subjects in both protocols.6,41,49,50 The day-to-day change in patterns of diurnal mood variation in a forced Inhibitors,research,lifescience,medical desynchrony protocol has remarkable similarities to the day-to-day variability in diurnal mood variation found in depressive patients, and even more similarity to the mood patterns

following a phase advance of the sleep-wake cycle.8 Thus, mood fluctuations can indeed be understood in terms of abnormal or changing Inhibitors,research,lifescience,medical phase relationships. Mood-related cognitive and attributional disturbances have been postulated to be sequelae of shifting circadian rhythms.5 ‘Ihis is an important point for the above findings. If SAD patients are vulnerable to short winter days, is this an abnormality of the biological clock, or is it rather a subjective interpretation of selleck Pacritinib internal temporal disorder? The following findings

are perhaps relevant to this argument. Some subjects in experiments where they live free of time cues manifest spontaneous internal desynchronization, in that their sleep-wake Inhibitors,research,lifescience,medical cycle desynchronizes from circadian rhythms such as core body temperature. They do not notice that this phenomenon has occurred, nor do they show any decrement in mood or performance―on the contrary, they feel rather Anacetrapib well.51 This is in marked contrast to the situation resulting from external desynchronization, when sleep timing is shifted by shift work or transmeridian travel. Here the internal desynchronization between sleep and the clock is additionally in conflict with light and social zeitgebers in the outer world; and it is postulated that this aspect may underlie the often-associated depressive disturbances.5,52 It may not only be phase relationships that are important, but perhaps also the light-dark ratio (daylength or photoperiod). Some of the evidence for SAD suggests that the duration of nocturnal melatonin secretion is important for triggering psychopathology in winter.