The Diagnosis, Symptomatology, and Epidemiology of Seasonal Affective Disorder

Abstract

The operational criteria for seasonal affective disorder (SAD) have undergone several changes since first proposed in 1984. SAD is currently included as a specifier of either bipolar or recurrent major depressive disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. The International Classification of Diseases, Tenth Edition has provisional diagnostic criteria for SAD. The most characteristic quality of SAD is that the symptoms usually present during winter and remit in the spring. Furthermore, the symptoms tend to remit when the patients are exposed to daylight or bright light therapy. The cognitive and emotional symptoms are as in other types of depression but the vegetative symptoms are the reverse of classic depressive vegetative symptoms, namely increased sleep and increased appetite. SAD is a common condition, but the exact prevalence rates vary between different studies and countries and is consistently found to be more common in women and in youth. SAD probably possibly occurs in children although not as commonly as in young adults. Some studies have found that certain ethnic groups who live at high northern latitudes may have adapted to the long arctic winter.

Coming to grips with complex disorders: Genetic risk prediction in bipolar disorder using panels of genes identified through convergent functional genomics

“…An increase in ARNTL gene expression was reported in postmortem brains from bipolar subjects [Nakatani et al, 2006]. Seasonal affective disorder (SAD), a variant of bipolar disorder [Magnusson and Partonen, 2005], is tied to the amount of daylight, which is a primary regulator of circadian rhythms and clock gene expression; associations between polymorphisms in the clock genes ARNTL, PER2, and NPAS2 and SAD have previously been reported [Johansson et al, 2003;Partonen et al, 2007]. Overall, ARNTL, RORB, DBP and related circadian clock genes are compelling candidates for involvement in bipolar disorders, acting as rheostats as well as underlying the core clinical phenomenology of cycling and switching from depression to mania [Bunney and Bunney, 2000;Wager-Smith and Kay, 2000;Niculescu et al, 2000b;Niculescu and Kelsoe, 2001;Kelsoe and Niculescu, 2002;Lenox et al, 2002;Hasler et al , 2006;Wirz-Justice, 2006;McClung, 2007;Le-Niculescu et al, 2008c].…”

Convergent functional genomics of genome‐wide association data for bipolar disorder: Comprehensive identification of candidate genes, pathways and mechanisms

“…Clock genes expression levels (Dbp, Per1, and Per2) have been reported to be changed by sleep deprivation in rodents [Wisor et al, 2002]. Seasonal affective disorder (SAD), a variant of bipolar disorder [Magnusson and Partonen, 2005], is tied to the amount of daylight, which is a primary regulator of circadian rhythms and clock gene expression; associations between polymorphisms in the clock genes Arntl, Per2, and Npas2 and SAD have previously been reported [Johansson et al, 2003;Partonen et al, 2007]. We had previously described the identification of clock gene D-box binding protein (Dbp) as a potential candidate gene for bipolar disorder [Niculescu et al, 2000b], using a CFG approach.…”

Abnormal Hypothalamic Response to Light in Seasonal Affective Disorder

“…W inter seasonal affective disorder (SAD) is a recurrent major depressive disorder occurring in fall/winter with full remission in spring/summer (1)(2)(3)(4). Patients with SAD tend to report typical depression complaints such as decreased mood and motivation but also atypical symptoms such as hypersomnia and fatigue, and hyperphagia (particularly for carbohydrates) associated with weight gain, which implies alteration in sleep/wake regulation (5,6) and possibly in metabolism (7).…”

“…Vulnerability to day-length shortening associated with fall/ winter is generally accepted as the main triggering factor of the disorder. Indeed, SAD prevalence varies with latitude (to reach up to 3% in Canada and possibly even up to 10% at higher latitude [2,4]), and light therapy is a treatment of choice for the disorder, with symptom improvements observed within a few weeks of daily (generally morning) light exposures (8). However, the mechanism linking exposure to light and mood regulation is still largely unknown.…”