Walsh Kate, Uddin Monica, Soliven Richelo, Wildman Derek E, Bradley Bekh
Columbia University Mailman School of Public Health, New York, NY 10032, United States.
Center for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48201, United States; Department of Psychiatry and Behavioral Neurosciences, Wayne State University, Detroit, MI 48201, United States.
J Affect Disord. 2014 Jun;161:91-6. doi: 10.1016/j.jad.2014.02.043. Epub 2014 Mar 12.
Prior studies have found that the 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene (SLC6A4) interacts with stressful life events to increase general risk for PTSD, but this association has not extended to African American samples. Further, little is known about the effects of this interaction on specific PTSD symptom clusters, despite indications that clusters may have different biological substrates. The current study examined the interaction between exposure to childhood emotional abuse and 5-HTTLPR genotype on risk for PTSD symptom severity and severity of specific PTSD symptom clusters in two African American samples.
Participants were 136 African American household residents from Detroit, MI and 546 African American patients recruited from waiting rooms in primary care clinics in Atlanta, GA. Participants reported emotional abuse exposure and PTSD symptom severity, and provided DNA for triallelic 5-HTTLPR genotyping. Analysis of covariance (ANCOVA) was used to examine main effects and interactions.
In both African American samples, 5-HTTLPR genotype modified the effect of emotional abuse on PTSD symptom severity. Participants with the low-expression SS genotype who were exposed to emotional abuse had significantly lower reexperiencing and arousal symptom severity scores.
The DNHS genetic sample size was small, and abuse data were assessed retrospectively.
The SS variant of 5-HTTLPR appears to buffer against developing the reexperiencing and arousal symptoms of PTSD in two independent African American samples exposed to childhood emotional abuse. Findings also highlight the importance of considering emotional abuse experiences in patients with suspected PTSD.
先前的研究发现,血清素转运体基因(SLC6A4)启动子区域的5-HTTLPR多态性与应激性生活事件相互作用,增加了患创伤后应激障碍(PTSD)的总体风险,但这种关联尚未扩展到非裔美国人样本。此外,尽管有迹象表明PTSD的不同症状群可能有不同的生物学基础,但对于这种相互作用对特定PTSD症状群的影响知之甚少。本研究在两个非裔美国人样本中,考察了童年期情感虐待暴露与5-HTTLPR基因型之间的相互作用对PTSD症状严重程度及特定PTSD症状群严重程度的影响。
参与者为来自密歇根州底特律的136名非裔美国家庭居民以及从佐治亚州亚特兰大初级保健诊所候诊室招募的546名非裔美国患者。参与者报告了情感虐待暴露情况和PTSD症状严重程度,并提供DNA用于5-HTTLPR三等位基因基因分型。采用协方差分析(ANCOVA)来检验主效应和相互作用。
在两个非裔美国人样本中,5-HTTLPR基因型均改变了情感虐待对PTSD症状严重程度的影响。暴露于情感虐待的低表达SS基因型参与者的再体验和觉醒症状严重程度得分显著更低。
底特律邻里健康研究(DNHS)的基因样本量较小,且虐待数据是通过回顾性评估的。
在两个暴露于童年期情感虐待的独立非裔美国人样本中,5-HTTLPR的SS变异体似乎可缓冲PTSD的再体验和觉醒症状的发展。研究结果还凸显了在疑似患有PTSD的患者中考虑情感虐待经历的重要性。