This is a seasonal circadian rhythm disorder which is four times more common in women than in men, is occasionally familial and is most frequent between the ages of 20 and 40 years. It is most prevalent in high latitudes where there is a greater seasonal change in the intensity and duration of exposure to light. Abnormalities of clock genes, for instance per 2, have been identified. They may change porphyrin metabolism which influences melatonin production.
The seasonal affective disorder develops during autumn and winter and remits in spring and summer, at which time there may even be mild hypomania. In the winter a DSPS pattern develops, associated with depression, an increase in appetite, particularly for carbohydrates, weight gain, fatigue and reduction in physical activity.
In the seasonal affective disorder there is slow elimination of circulating melatonin leading to a raised blood level in the mornings despite normal nocturnal secretion. The total sleep time increases, which is unlike other forms of depression, and the duration of both NREM and REM sleep increases, including stages 3 and 4 NREM sleep. The rhythm of cortisol secretion is phase delayed.
Seasonal affective disorder may be the extreme end of the normal range of seasonal variation in mood and behaviour. As winter approaches, the duration of the melatonin signal overnight lengthens and the abnormal elimination of melatonin initiates the DSPS.
Seasonal affective disorder responds to light therapy in up to 75% of patients, particularly if it is given on waking in the morning. Dawn simulation may be helpful and a combination of light therapy and exercise has been shown to be effective. Melatonin may help the depression slightly and this also responds transiently to sleep deprivation. Tricyclic and SSRI antidepressants are effective, but propranolol, which suppresses melatonin secretion, has no effect.
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