Serotonin Transporter Gene Promoter Polymorphism and Somatoform Symptoms
J Clin Psychiatry 2009;70(11):1536-1539
© Copyright 2015 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
Introduction: Symptoms of somatoform and affective disorders are thought to be connected to serotonergic neurotransmission because serotonin is known to regulate the functions relevant in these disorders, such as pain and mood. Previous studies have reported associations of these disorders with a functional polymorphism in the promoter region of the serotonin transporter gene, a limiting factor of the serotonergic neuronal system, as its alleles have been associated with differences in levels of synthesized transporter and therefore differences in reuptake efficiency.
Method: Ninety-one patients with at least 2 unexplained physical symptoms were clinically evaluated and genotyped for the triallelic genotypes of the serotonin transporter gene polymorphism; patients were recruited from 2001 until 2004. DSM-IV diagnoses were assessed using the International Checklists for ICD-10 and DSM-IV. Somatic complaints were quantified with an interview version of the Screening for Somatoform Symptoms, persistent symptoms in the last 2 years (SOMS-2) and the SOMS-7 (current symptoms in the last 7 days). Depressive symptoms were quantified with the Beck Depression Inventory (BDI).
Results: Subjects with higher-expressing allele variants of the serotonin transporter gene (L'L' and L'S') had significantly more somatic symptoms in the last 2 years (trait) than those with lower-expressing variants (S'S') (P < .01). No differences could be found in regard to short-term somatic symptoms (ie, in the last 7 days). Neither depressive symptoms nor a comorbid diagnosis of major depression was associated with allelic variants.
Conclusion: Somatoform symptoms may be associated with a functional polymorphism in the promoter region of the serotonin transporter gene.
Submitted: August 14, 2008; accepted October 9, 2008.
Online ahead of print: June 16, 2009.
Corresponding author and reprints: Anika Hennings, Philipps University of Marburg, Division of Clinical Psychology and Psychotherapy, Gutenbergstrasse 18, 35032, Marburg, Germany (firstname.lastname@example.org).