As we have described elsewhere, patients with seasonal affective disorder (SAD) have annually occurring cycles of depression in fall and winter alternating with euthymia or hypomania occurring in the spring or summer. In the past we have investigated the neurobiology of patients with SAD by studying their sleep and neuroendocrine functioning. We have found that they sleep longer and have reduced delta sleep in the winter, as compared with the summer. However, dexamethasone suppression of cortisol secretion and TSH release in response to externally injected TRH appear normal. This past year our neurobiological investigations have revolved around melatonin metabolism in SAD. Blood was drawn over a 48-hour period in 7 SAD patients and 7 normal volunteers both in summer and in winter in order to establish the pattern of melatonin secretion in patients and normals. In addition, the melatonin precursor, 5-hydroxy-tryptamine was administered orally to 10 patients and 10 normal volunteers in the winter months and blood was drawn over a 5 hour period for melatonin analysis. We hypothesized that perhaps SAD is characterized by melatonin overproduction and that such a load of melatonin precursor would result in greater production of melatonin in patients than in normals. The melatonin specimens have yet to be analyzed.
