边缘型人格障碍症状与生活压力事件:基因与环境相互作用的评估

Vilde Sofie Arneberg , Vilde Sundsvold , Ludvig Daae Bjørndal , Eivind Ystrom
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引用次数: 0

摘要

背景边缘型人格障碍(BPD)与高比率的生活压力事件(SLEs)有关。目前还不清楚在考虑了家族风险因素的影响后,经历过 SLE 的人是否会有更多的 BPD 症状。本研究的目的是:1)利用跨年龄和跨环境的压力源建立一个BPD预测模型;2)研究SLE是否会导致遗传和环境风险因素影响之外的更高水平的BPD症状。采用泊松回归法探讨哪些SLE可预测BPD症状。弹性净惩罚回归用于建立SLE和BPD症状的预测模型。为了区分环境因素和遗传因素,还进行了同卵双生子对照分析。加权多事件风险评分解释了症状总变化的 22%。共同的环境因素和遗传因素分别解释了 31% 和 47% 的 BPD 症状个体差异。测得的 SLE 可解释 42% 的 BPD 共同环境风险。在考虑了共同环境因素和遗传因素后,SLEs 对 BPD 的预测风险降低了。然而,SLE 增加的 BPD 症状风险超出了共同遗传和环境因素的影响。系统性红斑狼疮与 BPD 症状的关联主要是由于家庭环境的选择。确定导致系统性红斑狼疮和 BPD 症状的家族因素非常重要。系统性红斑狼疮与 BPD 症状的相关性仍然超出了遗传和环境因素的影响。
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Borderline Personality Disorder Symptoms and Stressful Life Events: An Evaluation of Gene-Environment Interplay

Background

Borderline personality disorder (BPD) is associated with high rates of stressful life events (SLEs). It is unclear whether people who experience SLEs have more BPD symptoms after accounting for the effects of familial risk factors. Our aims in the current study were to 1) create a predictive model of BPD using stressors across age and contexts and 2) examine whether SLEs resulted in higher levels of BPD symptoms beyond the effects of genetic and environmental risk factors.

Methods

The sample comprised 2801 twins from the Norwegian Institute of Public Health Twin Panel. Poisson regression was used to explore which SLEs predicted BPD symptoms. Elastic net penalized regression was conducted to develop a predictive model for SLEs and BPD symptoms. Co-twin control analyses were performed to differentiate between environmental and genetic factors.

Results

SLEs experienced during childhood and adulthood were associated with BPD symptoms. A weighted polyevent risk score explained 22% of the total variation in symptoms. Shared environmental and heritable factors explained 31% and 47% of individual differences in BPD symptomatology, respectively. Measured SLEs explained 42% of the shared environmental risk for BPD. The predictive risk of SLEs for BPD was reduced when shared environmental and genetic factors were accounted for. However, SLEs increased risk of BPD symptoms beyond the effects of shared genetic and environmental factors.

Conclusions

BPD symptomatology following SLEs cannot fully be explained by genetic and shared environmental factors. The SLE-BPD symptoms associations were primarily due to selection by family environments. It is important to identify familial factors that lead to both SLEs and BPD symptoms. SLEs remained associated with BPD symptoms beyond genetic and environmental confounding.
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来源期刊
Biological psychiatry global open science
Biological psychiatry global open science Psychiatry and Mental Health
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审稿时长
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