High social support buffers the effects of 5-HTTLPR genotypes within social anxiety disorder

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• 作者：Eva Reinelt (1)
  Maren Aldinger (1)
  Malte Stopsack (1)
  Christian Schwahn (2)
  Ulrich John (3)
  Sebastian E. Baumeister (4)
  Hans J?rgen Grabe (5)
  Sven Barnow (1)
  
• 关键词：Social anxiety ; Gene?×?environment interaction ; Social support ; 5 ; HTTLPR ; Serotonin transporter
• 刊名：European Archives of Psychiatry and Clinical Neuroscience
• 出版年：2014
• 出版时间：August 2014
• 年：2014
• 卷：264
• 期：5
• 页码：433-439
• 全文大小：219 KB
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• 作者单位：Eva Reinelt (1)
  Maren Aldinger (1)
  Malte Stopsack (1)
  Christian Schwahn (2)
  Ulrich John (3)
  Sebastian E. Baumeister (4)
  Hans J?rgen Grabe (5)
  Sven Barnow (1)
  
  1. Department of Clinical Psychology and Psychotherapy, Ruprecht-Karls-University, Hauptstra?e 47-51, 69117, Heidelberg, Germany
  2. Unit of Oral and Systemic Diseases, Department of Prosthodontics, Gerodontology and Dental Materials, Center of Oral Health, University of Greifswald, Greifswald, Germany
  3. Institute of Epidemiology and Social Medicine, University Medicine Greifswald, Walther-Rathenau-Str. 48, 17475, Greifswald, Germany
  4. Institute of Community Medicine, Ernst Moritz Arndt University, Walther-Rathenau-Str. 48, Greifswald, Germany
  5. Department of Psychiatry and Psychotherapy, Helios Hospital Stralsund, University Medicine Greifswald, Rostocker Chaussee 70, 18437, Stralsund, Germany
  
• ISSN：1433-8491

文摘

An interaction between genetic aspects and environmental stressors has been suggested with regard to the etiology of social anxiety disorder (SAD). However, potential protective interplays which might decrease the risk of SAD have not been considered so far. Thus, we analyzed the interaction between 5-HTTLPR and differing levels of social support regarding SAD. The sample was based on participants of the Study of Health in Pomerania, Germany. We used the triallelic genotype of 5-HTTLPR and longitudinal data of social support. Final analyses were conducted in 79 individuals with SAD and 1,708 without. The diagnosis of SAD was derived from diagnostic interviews in accordance with DSM-IV. Considering the risk of SAD, a general protective effect of high social support was shown independent of variation in 5-HTTLPR genotype. In contrast, the risk of SAD was increased for both genotypes within those individuals with low social support. Additionally, the odds ratio for suffering from SAD was about two times higher for carriers of the l/l genotype compared to those with at least one short allele in those perceiving less-supportive social environments. The findings suggest that SAD is influenced by a protective and a contributing gene?×?environment interaction. High social support might act in a protective and low social support in an increasing manner on the risk of SAD especially within carriers of the l/l genotype. Therefore, effects of 5-HTTLPR might be buffered by high social support with respect to the risk of SAD.