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Childhood trauma associated with short leukocyte telomere length in posttraumatic stress disorder.

机译:儿童创伤与创伤后应激障碍中白细胞端粒长度短有关。

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BACKGROUND: Posttraumatic stress disorder (PTSD) is associated with increased risk for age-related diseases and early mortality. An accelerated rate of biological aging could contribute to this increased risk. To investigate, we assessed leukocyte telomere length (LTL), an emerging marker of biological age, in men and women with and without PTSD. We also examined childhood trauma, a risk factor for both PTSD and short LTL, as a potential contributor to short LTL in PTSD. METHODS: Participants included 43 adults with chronic PTSD (n = 18 with multiple categories of childhood trauma) and 47 control subjects (none with multiple categories of childhood trauma) (mean age = 30.55, SD = 7.44). Exclusion criteria included physical illness, medication use, obesity, alcohol or substance abuse, and pregnancy. Structured clinical interviews were conducted to assess PTSD and other psychiatric disorders and childhood trauma exposure. LTL was measured with a quantitative polymerase chain reaction method. RESULTS: As predicted, participants with PTSD had shorter age-adjusted LTL than control subjects. Exposure to childhood trauma was also associated with short LTL. In fact, childhood trauma seemed to account for the PTSD group difference in LTL; only participants with PTSD and exposure to multiple categories of childhood trauma had significantly shorter LTL than control subjects. CONCLUSIONS: Childhood trauma is associated with short LTL in individuals with PTSD. Chronic exposure to the psychobiological sequelae of childhood trauma could increase risk for PTSD and short LTL. Thus, the lasting psychological impact of exposure to trauma in childhood might be accompanied by equally enduring changes at the molecular level.
机译:背景:创伤后应激障碍(PTSD)与年龄相关疾病和早期死亡的风险增加有关。生物衰老的速度加快可能导致这种风险增加。为了进行调查,我们评估了有和没有PTSD的男性和女性的白细胞端粒长度(LTL),这是生物年龄的新兴标志。我们还研究了儿童期创伤,这是PTSD和短LTL的危险因素,是造成PTSD短LTL的潜在因素。方法:参与者包括43名患有慢性PTSD的成人(n = 18,涉及多种儿童期创伤)和47名对照受试者(无,涉及多种类型的儿童期创伤)(平均年龄= 30.55,SD = 7.44)。排除标准包括身体疾病,药物使用,肥胖,酗酒或滥用药物以及怀孕。进行了结构化的临床访谈,以评估创伤后应激障碍和其他精神疾病以及儿童期创伤暴露。用定量聚合酶链反应法测量LTL。结果:正如预期的那样,PTSD参与者的年龄调整后的LTL比对照组的对象短。暴露于儿童期创伤也与短LTL有关。实际上,儿童期创伤似乎是造成LSD PTSD组差异的原因。只有患有PTSD并暴露于多种儿童期创伤的参与者的LTL明显短于对照组。结论:创伤后应激障碍患者的童年创伤与短LTL有关。长期暴露于儿童创伤的心理生物学后遗症可能会增加PTSD和短期LTL的风险。因此,儿童时期遭受创伤的持久心理影响可能伴随着分子水平上同样持久的变化。

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