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Journal of Personality Disorders

Publication date: 2010-08-01
Volume: 24 Pages: 427 - 444
Publisher: Guilford Press

Author:

Distel, Marijn A
Willemsen, Gonneke ; Ligthart, Lannie ; Derom, Cathérine ; Martin, Nicholas G ; Neale, Michael C ; Trull, Timothy J ; Boomsma, Dorret I

Keywords:

Science & Technology, Life Sciences & Biomedicine, Psychiatry, NETHERLANDS TWIN REGISTER, DSM-IV BORDERLINE, ASSESSMENT INVENTORY, CLASSICAL TWIN, RISK-FACTORS, LIFE EVENTS, CONCURRENT VALIDITY, CRITERIA, CHILDHOOD, ADOLESCENTS, Adolescent, Adult, Aged, Aged, 80 and over, Australia, Belgium, Borderline Personality Disorder, Diseases in Twins, Female, Genetic Predisposition to Disease, Humans, Impulsive Behavior, Male, Middle Aged, Models, Genetic, Models, Statistical, Multivariate Analysis, Netherlands, Personality Assessment, Risk Factors, Self-Injurious Behavior, Surveys and Questionnaires, Twins, Young Adult, 1701 Psychology, 5201 Applied and developmental psychology, 5203 Clinical and health psychology, 5205 Social and personality psychology

Abstract:

The patient population of borderline personality disorder (BPD) is heterogeneous; many different combinations of BPD symptoms can lead to a BPD diagnosis. We investigated to what extent the covariance among four main components of BPD is explained by shared genetic and environmental factors. Using an extended twin design, multivariate genetic models were applied to the scales of the PAI-BOR, a self-report questionnaire tapping four main features of BPD (affective instability, identity problems, negative relationships, and self-harm). Data on the four BPD scales were available for 5,533 twins and 1,202 siblings from the Netherlands, Belgium, and Australia. The correlations among the scales ranged from 0.23 to 0.50 and were best explained by a genetic common pathway model. This model specifies that genes and environment influence the covariance between four main features of BPD in qualitatively similar ways, through a single latent factor representing the BPD construct. The heritability of the latent BPD factor was 51% and the remainder of its variance was explained by unique environmental influences. For each BPD scale, except self-harm, around 50% of its variance was explained by the latent BPD factor. The remaining variance for each of the four scales was explained by genetic (4% for affective instability to 20% for self-harm) and environmental (38% for negative relationships to 67% for self-harm) factors that were specific to each scale.