The Implications of Genetic Studies of Major Mood Disorders for Clinical Practice
J Clin Psychiatry 2000;61(9):630-637
© Copyright 2017 Physicians Postgraduate Press, Inc.
Purchase This PDF for $40.00
If you are not a paid subscriber, you may purchase the PDF.
(You'll need the free Adobe Acrobat Reader.)
Receive immediate full-text access to JCP. You can subscribe to JCP online-only ($86) or print + online ($156 individual).
With your subscription, receive a free PDF collection of the NCDEU Festschrift articles. Hurry! This offer ends December 31, 2011.
If you are a paid subscriber to JCP and do not yet have a username and password, activate your subscription now.
As a paid subscriber who has activated your subscription, you have access to the HTML and PDF versions of this item.
Click here to login.
Did you forget your password?
Still can't log in? Contact the Circulation Department at 1-800-489-1001 x4 or send email
Background: This article is a selective review
and synthesis of relevant research findings from genetic studies
of major mood disorders and the application of these to clinical
Method: The article discusses the application of
genetic research findings in major mood disorders, including
epidemiologic and family study risk estimates, risk modifiers,
and the concepts of etiologic and phenotypic heterogeneity, to 3
clinical domains: risk counseling, diagnosis, and treatment
Results: Epidemiologic and family studies have
provided general risk estimates useful in counseling
mood-disordered patients and their relatives. A complete and
accurate family pedigree provides more individualized risk
estimates for specific cases and is useful in identifying the
phenotypic spectrum of the disorder being transmitted in the
family. Both proband course parameters and familial loading for
psychiatric illnesses may be relevant for the prediction of
treatment response. However, the hypothesis of inherited
pharmacologic selectivity remains to be proven.
Conclusion: Genetic studies of mood disorders
have not yet provided conclusive evidence of specific
susceptibility genes or their pattern of inheritance. However,
they have generated information that is useful to clinical