首页> 外文期刊>Translational psychiatry. >Affiliation buffers stress: cumulative genetic risk in oxytocin–vasopressin genes combines with early caregiving to predict PTSD in war-exposed young children
【24h】

Affiliation buffers stress: cumulative genetic risk in oxytocin–vasopressin genes combines with early caregiving to predict PTSD in war-exposed young children

机译:隶属关系缓解了压力:催产素-加压素基因的累积遗传风险与早期照料相结合,可以预测战争暴露的幼儿中的PTSD

获取原文
           

摘要

Research indicates that risk for post-traumatic stress disorder (PTSD) is shaped by the interaction between genetic vulnerability and early caregiving experiences; yet, caregiving has typically been assessed by adult retrospective accounts. Here, we employed a prospective longitudinal design with real-time observations of early caregiving combined with assessment of genetic liability along the axis of vasopressin–oxytocin (OT) gene pathways to test G × E contributions to PTSD. Participants were 232 young Israeli children (1.5–5 years) and their parents, including 148 living in zones of continuous war and 84 controls. A cumulative genetic risk factor was computed for each family member by summing five risk alleles across three genes ( OXTR , CD38 and AVPR1a ) previously associated with psychopathology, sociality and caregiving. Child PTSD was diagnosed and mother–child interactions were observed in multiple contexts. In middle childhood (7–8 years), child psychopathology was re-evaluated. War exposure increased propensity to develop Axis-I disorder by threefold: 60% of exposed children displayed a psychiatric disorder by middle childhood and 62% of those showed several comorbid disorders. On the other hand, maternal sensitive support reduced risk for psychopathology. G × E effect was found for child genetic risk: in the context of war exposure, greater genetic risk on the vasopressin–OT pathway increased propensity for psychopathology. Among exposed children, chronicity of PTSD from early to middle childhood was related to higher child, maternal and paternal genetic risk, low maternal support and greater initial avoidance symptoms. Child avoidance was predicted by low maternal support and reduced mother–child reciprocity. These findings underscore the saliency of both genetic and behavioral facets of the human affiliation system in shaping vulnerability to PTSD as well as providing an underlying mechanism of post-traumatic resilience.
机译:研究表明,创伤后应激障碍(PTSD)的风险是由遗传脆弱性和早期护理经历之间的相互作用所决定的。但是,通常通过成人回顾性帐户来评估看护情况。在这里,我们采用前瞻性纵向设计,结合早期护理的实时观察结果,并沿着加压素-催产素(OT)基因途径的轴线评估遗传责任,以测试G×E对PTSD的贡献。参加者为232名以色列幼儿(1.5-5岁)及其父母,其中包括148名生活在持续战争地区和84名控制人员。通过汇总先前与心理病理学,社交和护理相关的三个基因(OXTR,CD38和AVPR1a)的五个风险等位基因,计算每个家庭成员的累积遗传风险因子。诊断为儿童PTSD,并在多种情况下观察到母婴互动。在儿童中期(7-8岁),对儿童的心理病理学进行了重新评估。战争暴露使罹患Axis-I疾病的可能性增加了三倍:60%的暴露儿童到童年中期就表现出精神病,而62%的儿童表现出几种合并症。另一方面,产妇的敏感支持降低了精神病理学的风险。发现了G×E对儿童遗传风险的影响:在战争暴露的背景下,加压素-OT途径的更大遗传风险增加了心理病理学的倾向。在暴露的儿童中,从幼儿期到中期的PTSD慢性与较高的儿童,母体和父系遗传风险,较低的母体支持和更大的初始回避症状有关。孕产妇支持率低和母子互惠度降低预计可以避免孩子。这些发现强调了人类隶属系统的遗传学和行为学方面显着影响了PTSD的脆弱性,并提供了创伤后复原力的潜在机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号