In several studies we have found that treatment with bright environmental light, capable of suppressing human
melatonin, reverses the winter depressive symptoms of patients with
seasonal affective disorder (SAD), whereas light too dim to suppress human
melatonin is therapeutically ineffective. This finding, as well as the central importance of
melatonin as a hormonal mediator of photoperiodic changes on seasonal rhythms in animals, led us to test the hypothesis that
melatonin mediates the effects of shortening days on the winter symptoms of SAD and that the modification of
melatonin secretion by bright light mediates its
antidepressant effects. We partially reversed the
antidepressant effects of
phototherapy in 8 SAD patients by oral
melatonin administration, but in another study of 19 SAD patients we failed to find any therapeutic difference between the
beta-adrenergic blocker,
atenolol, which inhibits
melatonin secretion, and placebo. In a third study of 7 SAD patients we showed that the anti-depressant effects of
phototherapy were not photoperiodic and appeared to be independent of
melatonin suppression. There is some preliminary evidence that
melatonin secretion may be abnormal in SAD. We conclude that while
melatonin may play some role in the symptoms of SAD and the effects of
phototherapy, it cannot by itself account for these phenomena.