Psychiatric Times 
October 2005
Vol. XXII
Issue 11
Rosenthal et al. (1984) first described seasonal affective disorder (SAD) as a pattern of recurrent depressions with a winter onset and a full remission the following summer. The emergence of treatment, specifically light therapy, was met with a mixture of enthusiasm and cautious skepticism. However, there is now substantial evidence to support its efficacy. This paper will review the treatment of SAD with a focus on new developments in the area.
The clinical presentation of SAD frequently includes the prominence of reverse vegetative or atypical symptoms (Rosenthal et al., 1984). Of these symptoms, increased appetite, carbohydrate craving, weight gain and hypersomnia are most commonly reported in large samples of patients with SAD. Prevalence estimates suggest that the condition occurs in 1% to 3% of the North American population (Blazer et al., 1998; Levitt and Boyle, 2002) with a female to male sex ratio of 1.6:1 (Lam and Levitt, 1999). Although initial research seemed to suggest a high frequency of bipolar disorders among patients with SAD (Rosenthal et al., 1987; Thompson and Isaacs, 1988), this has not been confirmed in subsequent reports (Levitt and Boyle, 2002; Thalen et al., 1995; Wehr et al., 1991).
The etiology and pathophysiology of SAD are still unknown; however, various hypotheses have garnered prominence in the literature. Most notably among these hypotheses is the theory of a dysregulated circadian rhythm, causing a phase delay (Lewy and Sack, 1988). This theory has been supported by evidence that early-morning light therapy is superior to evening light therapy (Eastman et al., 1998; Lewy et al., 1998b; Terman et al., 1998).
Another pathophysiological explanation for SAD is the evidence that suggests a disruption of serotonergic neurotransmission. Human and postmortem studies suggest that serotonin metabolism is decreased during winter months (Brewerton et al., 1988). Further support for the serotonergic hypothesis derives from studies with selective serotonin reuptake inhibitors (Lam et al., 1995; Moscovitch et al., 2004) and the precipitation of depression in patients with SAD during tryptophan(Drug information on tryptophan) depletion studies (Lam et al., 1996; Neumeister et al., 1997). Specific candidate genes affecting the serotonin system have been examined, but the evidence is still mixed (Johansson et al., 2001; Rosenthal et al., 1998).
Other investigators have proposed other possible mechanisms including the role of melatonin(Drug information on melatonin) (Rosenthal et al., 1988), the photoperiod and latitudinal variation (Levitt and Boyle, 2002; Rosen et al., 1990), and the roles of other neurotransmitters (Oren et al., 1994; Rudorfer et al., 1993). However, there appears to be no single mechanism that can explain the syndrome entirely at this point in time.
Light Therapy
