{"title":"Borderline Personality Disorder Symptoms and Stressful Life Events: An Evaluation of Gene-Environment Interplay","authors":"Vilde Sofie Arneberg , Vilde Sundsvold , Ludvig Daae Bjørndal , Eivind Ystrom","doi":"10.1016/j.bpsgos.2024.100390","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>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.</div></div><div><h3>Methods</h3><div>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.</div></div><div><h3>Results</h3><div>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.</div></div><div><h3>Conclusions</h3><div>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.</div></div>","PeriodicalId":72373,"journal":{"name":"Biological psychiatry global open science","volume":"4 6","pages":"Article 100390"},"PeriodicalIF":4.0000,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biological psychiatry global open science","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2667174324001034","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
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.