IF WE KNEW the physiological cue for the annual change that triggers winter depression, the syndrome of seasonal affective disorder (SAD) would be validated, and there would be a rational basis for designing therapeutic interventions. The depressogenic effect of long winter nights coupled with the antidepressant effect of morning light therapy make for a plausible story line. In this issue of the ARCHIVES, Wehr et al1 at the National Institute of Mental Health (NIMH) report that the melatonin secretion profile, an internal correlate of night length controlled by the hypothalamic biological clock, is linked to emergence and remission of the depression. By aggregating the largest sample size ever for such a study (55 patients and matched controls), they are able to derive virtually noise-free melatonin curves with a set of discrete anchor points: secretion onset and offset as well as final daytime clearance of the hormone from blood circulation.
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