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The Roscommon Family StudyIV. Affective Illness, Anxiety Disorders, and Alcoholism in Relatives
Kenneth S. Kendler, MD;
Mary McGuire, MB, MRCPsych;
Alan M. Gruenberg, MD;
Aileen O'Hare, MSocSci;
Mary Spellman, MB, MRCPsych;
Dermot Walsh, MB, FRCPI
Arch Gen Psychiatry. 1993;50(12):952-960.
Abstract
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Objectives
This report seeks to evaluate the specificity of the familial liability to schizophrenia by examining in the relatives of the various proband groups the risk for affective illness (AI), anxiety disorders, and alcoholism.
Design
A case-controlled epidemiologic family study using DSM-III-R criteria.
Participants
Three hundred eighty-four index probands from a psychiatric case register, 150 unselected control probands from an electoral register and 2043 of their living and traceable relatives, of whom 1753 were personally interviewed.
Results
In personally interviewed relatives of schizophrenic probands, the lifetime risk for all AI (24.9%±3.8%) or just bipolar AI (1.2%±0.7%) was very similar to that found in interviewed relatives of controls (22.8%±4.0% and 1.4%±0.7%, respectively). However, the risk for all AI (49.7%±12.9%) or bipolar AI (4.8%±3.2%) was sub- stantially increased in relatives of schizoaffective probands. A substantially higher proportion of relatives of schizophrenic vs control probands who had AI demonstrated psychotic—andmood-incongruentpsychotic— symptoms when affectively ill. Neither the risk for anxiety disorders nor that for alcoholism was increased in relatives of schizophrenic vs control probands.
Conclusions
The familial liability to schizophrenia possesses some specificity and does not substantially increase the risk to AI, anxiety disorders, or alcoholism. Even when narrowly defined, schizoaffective disorder has a substantial familial link to classic AI. The familial liability to schizophrenia predisposes to psychosis, and especially moodincongruent psychosis, when affectively ill. Finally, these results do not support the hypothesis that, from a familial perspective, schizophrenia and AI are on a single etiologic continuum.
Author Affiliations
From the Departments of Psychiatry and Human Genetics, Medical College of Virginia/Virginia Commonwealth University, Richmond (Dr Kendler); St Patrick's Hospital and the Western Health Board, Castlerea, Ireland (Drs McGuire and Spellman); Dave Garroway Laboratory for the Study of Depression, Pennsylvania Hospital, and Department of Psychiatry, University of Pennsylvania School of Medicine, Philadelphia (Dr Gruenberg); The Health Research Board, Dublin, Ireland (Ms O'Hare and Dr Walsh); and St Loman's Hospital, Dublin (Dr Walsh).
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