Although it has been established that bright light is an effective treatment for SAD, the mechanism of its action remains unknown, as do the fundamental biological abnormalities responsible for the syndrome. In previous years we have demonstrated biological abnormalities in patients with SAD and effects of light on a wide variety of biological systems. This past year we have extended these studies and, in particular, have conducted studies to examine two specific hypotheses involving the circadian system, and one involving the brain serotonergic systems. Circadian theories of SAD and phototherapy hold that there is an abnormality of either timing or amplitude of circadian rhythms, which is restored to normality by appropriately timed exposure to bright environmental light. We have shown abnormally low nocturnal secretion of melatonin, prolactin, TSH and growth hormone in SAD patients, which support the low amplitude hypothesis, as does our finding that the amplitude of the circadian rhythm of core body temperature is enhanced by bright light treatment. On the other hand, we have shown no abnormality in timing of circadian rhythms of these hormones, and no significant shift of these hormones following effective light therapy. Oral administration of the serotonin-2 antagonist, metergoline was given to eight SAD patients who were receiving phototherapy. No change of symptoms was seen with this drug, as compared to placebo, a finding that failed to advance further the serotonergic hypothesis of SAD and light therapy.
