ABSTRACT Seasonal affective disorder (SAD) is characterized by annual recurrence of clinical depression in the fall and winter months. The importance of SAD as a public health problem is underscored by its high prevalence (an estimated 5%) and by the large amount of time individuals with SAD are impaired (on average, 5 months each year). The specific cause of SAD remains unknown; however, researchers have identified possible chronobiological and psychological vulnerabilities to SAD. The study aimed to clarify psychological and chronobiological correlates of SAD in the first test of an integrative model of SAD. The project used a longitudinal design to test the respective contributions of the chronobiological and cognitive vulnerabilities on winter depression severity in 31 SAD patients and 33 never-depressed controls at sites in Burlington, VT and Pittsburgh, PA. The measures selected for the cognitive vulnerability were established measures of vulnerability to nonseasonal depression with empirical support for their relevance to SAD: brooding rumination, dysfunctional attitudes, cognitive reactivity to an induced sad mood, and season-specific cognitions. The chronobiological vulnerability was measured as Phase Angle Difference (PAD) and deviation from PAD of 6 hours. All measures were completed once in the summer, when the SAD patients were remitted, and once in the winter, when patients were clinically depressed. Patients were distinguished from controls on most cognitive vulnerability measures (brooding, as well as rumination, dysfunctional attitudes, and seasonal beliefs). SAD patients exhibited shorter PAD than controls, but did not exhibit greater deviation from PAD-6. Results provide further support for specific cognitive, but not chronobiological, vulnerabilities in prediction of SAD. Limitations of the current sample are discussed. Results hold implications for future SAD research bridging the chronobiological and psychological disciplines with the ultimate aim of improved understanding, assessment, treatment, and prevention of SAD.

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Thesis (M.A.)--York University, 2007. Graduate Programme in Kinesiology and Health Science. / Typescript. Includes bibliographical references (leaves 53-72). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR38808

Thesis (Ph.D.) in Psychology--University of Maine, 2003. / Includes vita. Includes bibliographical references (leaves 117-135).

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The short dark days of winter, related lack of energy, and low mood have always been part of life for those living in northern latitudes. For many, the gradual changes of the seasons are accompanied by the gradual degradation of their mental health. This disruptive effect is called Seasonal Affective Disorder (SAD). It is defined as major depressive episodes characterized by their seasonal recurrence for at least 2 consecutive years. Symptoms generally involve fatigue and a severe lack of energy leading to difficulty in performing daily activities as well as increased worry, anxiety, and irritability. Product Design in the field of SAD is positioned primarily in the treatment phase. Bright Light Therapy (BLT) products are used to attempt to alleviate the symptoms of the disorder. Efforts should focus on the prevention of mental illness to have a holistic impact on sustainable development. This project aims to identify an innovation opportunity where Product Design can be leveraged to prevent SAD. By leveraging semiotics, the study of signs and how meanings are created, in the field of lighting and design, a concept was developed that aims at complementing existing regulations in providing users with the conditions for improved well-being in the home. SAD is strongly linked to natural light and its cycles. Windows, the main provider of this kind of light in the home, have practical, comfort- and information-related roles. The developed concept aims at enhancing the meaning of windows to highlight our dependency on natural light cycles and prevent SAD. To effectively evaluate the concept and its effectiveness in creating meaning, it must be further developed and exposed to potential users.

Family and twin studies have shown a heritable component to seasonal affective disorder (SAD). While a few studies have examined individual genetic variants in SAD, many methodological issues exist in the current literature. First, most studies combined major depression (MDD) and bipolar (BD) cases in the genetic analysis of SAD. This makes it difficult to differentiate the effect from MDD and BD. Second, most studies adopted a candidate gene approach and used fairly small sample sizes. This does not allow for testing across a wide variety of genes, and it yields less robust P-values. Third, healthy controls have been used, but not case comparisons, which makes it difficult to differentiate the effects of seasonality from that of the primary illness (MDD and BD). To overcome these issues, seasonal MDD and BD cases were separated into two different studies in this thesis; sample sizes for both studies are the largest in the current SAD molecular genetics literature; GWAS was used to test for potential risk loci in a hypothesis-free fashion; case comparisons were incorporated to exclude potential genetic contributions related generally to the primary diseases themselves (MDD and BD). For MDD, we performed a GWAS with 562 seasonal MDD cases and 1,225 comparison cases with non-seasonal MDD. Subjects were drawn from two iterations of the Genetics of Recurrent Early Onset Depression (GenRED) study. Seasonal cases were those whose depressive episodes typically started in fall or winter. A mega-analysis of the two GWAS datasets was done using SNPTEST. We found that two single nucleotide polymorphisms (SNPs), rs149882931 and rs77073398, on chromosome 16p12.1 were associated with seasonal depression, at a genome-wide significant level (OR= 1.66, P= 3.59 x 10-8 and OR=1.62, 4.76 x 10-8, respectively). Since SAD is more prevalent in females, a female-specific analysis was carried out. The two variants were more significant in this analysis: P=2.18x10-9 (OR=1.89) and P=2.79x10-9 (OR=1.82), respectively, and a significant sex-by-SNP interaction was observed. These SNPs are located in a conserved intergenic region between the genes HS3ST4 and C16orf82. The protein product of HS3ST4 modifies the side chains of heparan sulfate proteoglycans. We therefore tested the hypothesis that the heparan sulfate biosynthesis pathway would be enriched in nominally significant SNPs using the SNP ratio test, and found evidence for such enrichment (P=0.008, SNP ratio test, P=0.027, SKAT). For BD, the GWAS analysis of 818 seasonal BD cases and 1,515 healthy controls showed that BD-S is most strongly associated with two SNPs within the ZBTB20 genes. BD subjects were drawn from NIMH Bipolar Genetics Study (BIGS), and seasonal cases were defined as those with depressive episodes starting in fall or winter. An association study was carried out with SNPTEST, and we found two single nucleotide polymorphisms (SNPs) in the intronic region of ZBTB20 gene to be associated with BD-S (rs7646282, OR=2.34, P= 7.23 x 10-8 and rs139459337, OR=2.37, 8.05 x 10-8). A similar case-only study was carried out with 818 BD-S cases and 1239 cases without seasonal depressive symptoms (non-BDS), though no SNP was found to be significantly associated in this analysis. rs7646282 is the strongest SNP in cis-association with ZBTB20 gene expression, and ZBTB20 has been shown to affect the neural development of the hippocampus, a brain region implicated in the pathophysiology of BD. Finally, we sought to determine whether there is a role for circadian rhythm genes in BD susceptibility. In this study, we used a discovery set of 189 exome-sequenced BD patients and 105 healthy controls to look for circadian genes associated with BD. We found the DRD2 gene to be the circadian gene most strongly associated with BD. Among the rare damaging variants in the DRD2 gene, the S311C variant was the predominant SNP. To test whether this variant segregates in family members with BD, we genotyped the family members of probands from the discovery sample. This data was used for a linkage and family-based association study. Even though the linkage analysis was only very weakly positive, the family-based association study showed significant segregation of the variant in family members with BD (P< 0.05). To follow up on this finding, we further genotyped 2,185 unrelated BD cases and 1,982 healthy controls. We found no support for the S311C variant in this replication dataset. Sub-phenotype study of psychotic features and mood-incongruence also did not show significant association. Meta-analysis with 2,994 BD cases and 3,661 controls, however, revealed no association between the S311C variant and BD.

The changes of the seasons are a phenomenon we as people in many cases are affected by multiple times a year. However, how much this change affects us differs from where in the world you live. In the northern hemisphere, life can change drastically when the sun goes from shining the majority of the day to the day being mostly in darkness during wintertime. Most people are affected by this change somehow, especially the change from brighter days to darker. This is when feelings of community, hopefulness and happiness can be switched out with feelings of loneliness, malaise and even depression. This paper shows that although not all people experience the changes in these black-or-white ways, it is clear that the gray area between not being affected at all or shutting down completely is large and sometimes hard to define.  In this study, we have examined the general outlook towards winter darkness and the experiences of students at Umeå University, Sweden, who moved here from a more southern part of Sweden where the darkness is not as drastically changing during wintertime. We also interviewed the student health team at Umeå University to gain knowledge about however this is something they are working actively against or not. / Förändringarna i årstid är något vi människor utsätts för flera gånger varje år, men hur denna förändring ser ut skiljer sig väldigt mycket beroende på var i världen man bor. I den nordliga delen av världen förändras livet väldigt mycket då man går från sol större delen av dagen till mörker större delen av dagen under vintertid.  De flesta människor påverkas av denna förändring i årstid, framförallt den förändring där vi går ifrån ljusare tider mot mörkare. Här kan känslor av gemenskap, hoppfullhet och lycka bytas ut mot känslor av ensamhet, nedstämdhet och depression. Uppsatsen visar att alla människor självklart inte lider av säsongsförändringarna på detta svart-eller-vitt sätt. I spektrumet av att inte påverkas alls till att sluta fungera på grund av säsongsförändringar så är det tydligt att det finns flera olika svar på hur människor påverkas.  I vår studie har vi undersökt inställningen till vintermörkret och upplevelserna hos studenter på Umeå universitet som flyttat upp till Norrland samt att vi har intervjuat Studenthälsan på Umeå Universitet för att se huruvida detta är något de arbetar aktivt mot.

Tidigare studier visar på ett samband mellan årstidsbunden depression och underprissättning vid börsintroduktioner på den amerikanska marknaden. Studien undersöker detta samband på börsintroduktioner genomförda i Sverige, där prevalensen av årstidsbunden depression är hög. Prevalensen och effekten av årstidsbunden depression skattas genom dagslängd och förändringen av dagslängden. För att besvara forskningsfrågan utförs tre regressionsanalyser på studiens urval bestående av 147 börsintroduktioner genomförda år 2006 till 2019 på Nasdaq OMX Stockholm och Nasdaq First North. Resultatet visar en genomsnittlig underprissättning på 8,2%. Däremot uppvisas inget signifikant samband mellan årstidsbunden depression och underprissättning.

Many of us can relate to being tired and maybe even feel down during the winter months. Reports show that we spend more and more time indoors and with that, problems linked to low daylight exposure increases. The main recommendation from doctors is to try to spend more time outdoors to really get that dosage of the sun that one needs. Research also shows that people are not aware of the actual amount of time they spend either indoors or in their cars.  With this in mind, what could we do to create a healthier way of living?  In this project, I have chosen to explore how we can motivate and inspire people with a sensitivity to light to spend more time outdoors and help them stimulate their circadian rhythm. People that suffer from symptoms could in worst cases not even leave their bed making them unable to cope with their life. Using natural ways of changing habits could in most cases have a better effect than what heavy medication does.