Last year we showed that exogenously administered melatonin reinduced some but not all the symptoms of SAD, which had responded to phototherapy in 8 patients with SAD. This year we treated 18 patients with SAD with the beta-blocker, atenolol, which has been shown to suppress melatonin secretion. We found that in the population as a whole there was no significant difference between the effects of melatonin and of placebo. However, some patients appeared to do extremely well on atenolol throughout the winter months. These patients relapsed when atenolol was discontinued and responded once again when it was reinstated. It is possible that there is a subgroup of patients with SAD in whom the secretion of melatonin plays an important role in the pathogenesis of their symptoms. The study of skeleton photoperiod treatments in 7 patients with SAD also suggests that melatonin secretion may not play a major role in the pathogenesis of SAD in most patients. Naturalistic studies of plasma melatonin profiles over a period of 48 hours have been conducted in 7 SAD patients and 7 normals in both summer and winter and these samples await analysis. It is not clear at this time what role melatonin secretion has in the pathogenesis of SAD or in the response of this condition to phototherapy. Some of our studies suggest that melatonin has some role in these processes, at least in certain patients. However, all studies argue against a major role for melatonin in the population as a whole and the skeleton photoperiod study, which is perhaps the most clearly negative one, raises the possibility that melatonin secretion has no role at all.
