Seasonal variations in mood and behavior (seasonality) and seasonal affective disorder (SAD) have been attributed to seasonal fluctuations in brain serotonin (5-HT). 1 the short (s), as opposed to the long (l), allele of the 5-HT transporter linked polymorphism (5-HTTLPR) has been associated with neuroticism and depression. 2,3 We hypothesized that this short allele would also be associated with SAD and with higher levels of seasonality. Ninety-seven SAD patients and 71 non-seasonal healthy controls with low seasonality levels were genotyped for 5-HTTLPR and compared statistically. Patients with SAD were less likely to have the l/l genotype (27.8% vs 47.9%; P Ͻ 0.01) and more likely to have the s allele (44.8% vs 32.4%; P Ͻ 0.02) as compared to controls. The three 5-HTTLPR genotypes were also differentially distributed in patients and controls (P Ͻ 0.03). The SAD patients with the l/l genotype had a lower mean seasonality score than did patients with the other two genotypes (mean ± s.d. = 15.3 ± 2.8 vs 17.1 ± 3.4 respectively; P Ͻ 0.02). The 5-HTTLPR short allele contributes to the trait of seasonality and is a risk factor for SAD, providing further evidence for a relationship betwen genetic variation in the 5-HT transporter (5-HTT) and behavior.The tendency for the majority of individuals in temperate latitudes to experience changes in behavior across the seasons has been termed seasonality. 4 Seasonality, as measured retrospectively by self-report, is a heritable trait 5 which varies in severity across individuals. Seasonality is present to a marked degree in patients with seasonal affective disorder (SAD), a condition of regularly recurring winter depressions alternating with non-depressed periods in spring and summer. 6 Although depression is also heritable, it is unclear whether SAD is inherited as a distinct entity or whether it affects individuals who are genetically susceptible to both seasonality and depression.SAD has been hypothesized to result from disturbed brain serotonergic transmission 1 and patients with SAD have been shown to respond abnormally to drugs that act on serotonin (5-HT) receptors and favorably to antidepressants that block the 5-HTT. 1 Seasonal fluctuations in 5-HT hypothalamic concentration have been reported post-mortem in the general population, with lowest levels occurring in winter. 7 As the behaviors that vary with the seasons, including appetite, sleep, weight regulation and mood, are controlled in part by 5-HT pathways, seasonality may also be related to seasonal fluctuations in 5-HT function.Given the importance of the 5-HTT in modulating 5-HT transmission 2 in the 5-HT synapse, variations in 5-HTT regulation may account for variations in seasonality in the general population and may be a risk factor for SAD. A polymorphism of the promoter of the 5-HTT gene [SCL6A4 localization on chromosome 17q12] has recently been described. 2 The polymorphism is an insertion or deletion of a 44-bp sequence located approximately 1 kb upstream from the coding sequence. The l and s variants...

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The purpose of this study was to ascertain whether men and women with seasonal affective disorder (SAD) differ in their clinical presentation or in their response to bright light therapy. Data from all patients who participated in our SAD clinic between 1981 and 1991 were analyzed retrospectively. A linear discriminant function analysis was performed using self‐report data from the Seasonal Pattern Assessment Questionnaire and the Seasonal Screening Questionnaire (N =167 women and 43 men). SIGH‐SAD ratings (consisting of the Hamilton Depression Rating Scale and an addendum for atypical symptoms) were analyzed to determine if men and women differed in clinician‐rated symptoms at baseline (N = 86 women and 28 men), or in their response to phototherapy (N =43 women and 16 men). Male and female SAD patients did not differ in clinician‐rated symptoms or in their response to phototherapy. However, on self‐report scales, men reported more severe illness, while women reported more carbohydrate craving, a greater percentage increase in weight, and more hours of sleep per night in the winter. The linear discriminant function analysis correctly classified 93.4% of the women but only 27.9% of the men. Since we found significant differences only on self‐report scales, our results may reflect a gender difference in symptom reporting. Alternatively, our findings may reflect gender differences in depressive symptomatology or differences between normal men and women in the sleep‐wake cycle or in carbohydrate craving. Men with SAD may have a more heterogeneous presentation than women with SAD. There is, however, no gender difference in response to phototherapy. Depression 3:13–19 (1995). © 1995 Wiley‐Liss, Inc .

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