The etiology and pathophysiology of seasonal affective disorder (SAD) has been linked to the seasons and to light since its first conceptualization. Aspects of SAD that make it particularly amenable to biological investigation include the predictable recurrent episodes, the rapid response to a nonpharmacologic treatment, the specific neurovegetative features, and the availability of rich animal models of seasonality. This paper reviews new findings for the major biological hypotheses for SAD, focusing on circadian rhythms, neurotransmitters, and molecular genetics. Integrative issues and future directions for the study of SAD, including the heuristic value of a dualvulnerability hypothesis that conceptualizes seasonality as a dimensional construct and the importance of studying endophenotypes, will be discussed.

These results suggest that changes in various sociocultural aspects have increased the risk of developing eating disorders in Korea, and support the sociocultural hypothesis of eating disorders.

OXC was effective and well-tolerated in refractory BD and schizoaffective disorder. These preliminary data are promising but controlled studies are needed to confirm its efficacy in refractory BD.

Evidence-based treatments for seasonal affective disorder (SAD) include light therapy and pharmacotherapy. We briefly review the diagnosis and treatment of SAD, focusing on clinical and treatment differences between patients with unipolar and bipolar illness. Special considerations for the management of SAD in patients with bipolar disorder are discussed, including the need to monitor for emergence of manic and hypomanic mood switches, to use mood stabilizers in patients with bipolar I disorder, and to be aware of potential interactions between bright light and medications used in treating bipolar disorder. Chronobiological treatments such as bright light therapy may be combined with pharmacotherapy to enhance therapeutic effects, reduce adverse side effects, and optimize treatment in patients with seasonal and nonseasonal bipolar disorder.