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Editorial
Mood Disorders—New Definitions, New Treament Directions
Paul Grof
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In Review
"Cade's Disease" and Beyond: Misdiagnosis, Antidepressant Use, and a Proposed Definition for Bipolar Spectrum Disorder
S Nassir Ghaemi, James Y Ko, Frederick K Goodwin
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The Neurobiology of Bipolar Disorder: Focus on Signal Transduction Pathways and the Regulation of Gene Expression
Yarema Bezchlibnyk, L Trevor Young

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Original Research
Major Depression and Its Association With Long-Term Medical Conditions

Lisa M Gagnon, Scott B Patten

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Seasonal Affective Disorders: Relevance of Icelandic and Icelandic-Canadian Evidence to Etiologic Hypotheses
Jóhann Axelsson, Jón G Stefànsson, Andrés Magnússon, Helgi Sigvaldason, Mikael M Karlsson

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Canadian Psychiatric Inpatient Religious Commitment: An Association With Mental Health
Marilyn Baetz, David B Larson, Gene Marcoux, Rudy Bowen, Ron Griffin

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The Moderating Effects of Coping Strategies on Major Depression in the General Population
JianLi Wang, Scott B Patten

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Antidepressant Side Effects in Depression Patients Treated in A Naturalistic Setting: A Study of Bupropion, Moclobemide, Paroxetine, Sertraline, and Venlafaxine
JD Vanderkooy, Sidney H Kennedy, R Michael Bagby

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Treatment Delays for Involuntary Psychiatric Patients Associated With Reviews of Treatment Capacity
Michelle Kelly, Sandra Dunbar, John E Gray, Richard L O'Reilly

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Book Reviews
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Books Received

Letters to the Editor
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Original Research

Seasonal Affective Disorders: Relevance of Icelandic and Icelandic-Canadian Evidence to Etiologic Hypotheses

Jóhann Axelsson, PhD, DPhil1, Jón G Stefánsson, MD2, Andrés Magnússon, MD, PhD3,
Helgi Sigvaldason, PhD4, Mikael M Karlsson, PhD5

 

Objective: This study tests the suggestion of earlier studies concerning the importance of genetic factors in the etiology of winter seasonal affective disorders (SADs) and subsyndromal winter SAD (S-SAD).

Method: Two study populations of Winnipeg, Manitoba residents were canvassed: 250 adults of wholly Icelandic descent and 1000 adults of non-Icelandic descent. We distributed the Seasonal Pattern Assessment Questionnaire by mail to these 2 populations, yielding 204 and 449 valid responses, respectively.

Results: Rates of SAD and S-SAD proved markedly lower in the Icelandic population than those in the non-Icelandic population.

Conclusions: These differences seem unexplained by differences in ambient light or climate, thus indicating that genetic factors contribute to the expression of SADs. Compared with earlier findings from a group of adults of wholly Icelandic descent living in nearby rural Manitoba, the etiologic importance of as-yet-undetermined environmental factors unrelated to latitude or ambient light is also indicated.

(Can J Psychiatry 2002;47:153–158)

Clinical Implications:

  • This study points out the inadequacy of the etiologic component of the latitude hypothesis in explaining winter seasonal affective disorders (SADs).
  • The study implies that SADs are importantly dependent upon genetic factors.
  • The study suggests that SADs are also dependent upon non-light-related environmental factors.

Limitations

  • The study relies upon genealogic and anthropometric data in assessing genetic similarity.
  • The study leaves unexplained the similarity in prevalences of SAD and SAD plus S-SAD in Icelandic populations in Manitoba and in Iceland, despite the large difference in latitude between the places of residence of these populations.
  • The present study does not isolate the non-light-related environmental factors which evidently play a role in the expression of SADS

Key Words: SAD, seasonal affective disorder, seasonal disorder, affective disorder, mood disorder, depression, comparative study

Résumé : Troubles affectifs saisonniers : utilité des données probantes islandaises et islando- canadiennes des hypothèses étiologiques


Seasonal Affective Disorder (SAD), in the sense discussed here (sometimes called winter SAD), is a depression which occurs regularly in fall and winter, with remission during spring and summer (1,2).

Most epidemiologic research on SAD has made use of the Seasonal Pattern Assessment Questionnaire (SPAQ), an instrument developed by Rosenthal and his colleagues (3), and of the SPAQ criteria for SAD, which Kasper and associates subsequently developed (4). Subsyndromal winter SAD (S-SAD), a milder form of the disorder, has also been described (4,5).

In a well-known study, Rosen, Rosenthal, and coworkers used the SPAQ to determine prevalences of SAD and S-SAD at 4 locations along the US eastern seaboard: Sarasota, Florida (latitude 27°N); Montgomery County, Maryland (latitude 39°N); New York City (latitude 40°N); and Nashua, New Hampshire (latitude 42.5°N) (6). They found that prevalences of SAD and S-SAD correlated positively with latitude, and this accorded with earlier surveys, not based upon the SPAQ (7,8).

The idea that prevalences of SAD and S-SAD vary directly with latitude, due to the inverse variation of winter ambient light with latitude, may for convenience be styled the “latitude hypothesis” (9).

 

This hypothesis has 2 separable elements: a descriptive element (direct variance of prevalence with latitude) and an etiologic element (light deprivation as a principal causal factor). Aside from the support derived from the empirical findings reviewed above, the latitude hypothesis gains credibility from the fact that both SAD and S-SAD respond well to phototherapy (1,4, 5,10–14), as summer SAD does not (15,16).

In 1993, Magnússon and Stefánsson published the results of a study on SAD and S-SAD, which was conducted in Iceland using Rosenthal’s methods (11). Iceland is located at 63.4º to 66.5ºN latitude. This study revealed that the prevalence rates for SAD and S-SAD were markedly lower in Iceland than those found in 3 of the American locations studied by Rosenthal—locations that lie 21º to 27.5º to the south of Iceland. In addition, Magnússon and Axelsson (9) found that the combined prevalence of SAD plus S-SAD in Manitobans of wholly Icelandic descent (living at approximately 50.5ºN latitude) was only marginally higher than that reported by Rosenthal and coworkers from Sarasota, Florida, lying 23.5° to the south. These findings contradicted the latitude hypothesis in any simple form and suggested that genetic factors might play an important causal role in SAD and S-SAD—an idea subsequently corroborated by other researchers (17–19).