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首页> 外文期刊>European archives of psychiatry and clinical neuroscience >High social support buffers the effects of 5-HTTLPR genotypes within social anxiety disorder
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High social support buffers the effects of 5-HTTLPR genotypes within social anxiety disorder

机译:较高的社会支持度可以缓解5-HTTLPR基因型在社交焦虑症中的作用

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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.
机译:关于社交焦虑症(SAD)的病因,已提出遗传因素和环境压力因素之间的相互作用。但是,到目前为止尚未考虑可能降低SAD风险的潜在保护性相互作用。因此,我们分析了5-HTTLPR与不同水平的SAD社会支持之间的相互作用。该样本基于德国Pomerania的健康研究参与者。我们使用了5-HTTLPR的三倍体基因型和社会支持的纵向数据。对79位SAD患者和1,708位SAD患者进行了最终分析。 SAD的诊断是根据DSM-IV从诊断性访谈中得出的。考虑到SAD的风险,显示出高社会支持的一般保护作用,而与5-HTTLPR基因型的变化无关。相反,在社会支持率低的个体中,两种基因型的SAD风险均增加。此外,在那些对社会支持程度较低的人群中,l / l基因型携带者患SAD的几率比那些具有至少一个短等位基因的携带者高出约两倍。研究结果表明,SAD受保护性基因和环境基因相互作用的影响。较高的社会支持可能会以保护性和较低的社会支持以增加的方式对SAD风险起作用,尤其是在l / l基因型携带者中。因此,就SAD风险而言,较高的社会支持可能会抑制5-HTTLPR的影响。

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