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Introduction
Borderline personality disorder (BPD) is a severe personality disorder whose features include impulsivity, affective instability, relationship problems and identity problems (APA, 2000). BPD is associated with interpersonal and occupational impairment, increased risk for suicide and higher rates of treatment in both medical and psychiatric settings (Skodol et al. 2002). In addition, BPD is frequently co-morbid with Axis I disorders, especially substance use disorders in males, eating disorders in females, anxiety disorders and mood disorders (Zanarini et al. 1998; Zimmerman & Mattia, 1999), and this co-morbidity predicts poorer short- and long-term outcome (Skodol et al. 2002).
Most of our knowledge about BPD has been obtained through the study of clinical samples. Clinical samples are important for characterizing the syndrome as it typically is presented for treatment, assessing the longitudinal course of the disorder, and evaluating the disorder's response to forms of treatment. However, clinical samples are limited in their ability to address certain important epidemiological and aetiological questions as they are likely to contain more severe cases and may therefore not be representative of the disorder as it appears in the general population. Also, these clinical cases often exhibit more co-morbidity than cases from the community (Skodol et al. 2002), thereby further clouding the aetiological picture. In addition to clinical studies, it is therefore informative to identify BPD features in the general population to gain a full understanding of the nature of BPD and the developmental pathways leading to BPD.
One important aetiological issue for which community samples are essential is the degree to which there is a genetic influence on the manifestation of BPD symptoms. Increased rates of BPD have been found in the relatives of individuals with BPD (e.g. Loranger et al. 1982; Baron et al. 1985; Johnson et al. 1995; Zanarini et al. 2004), and the heritability of traits that are highly associated with BPD (e.g. neuroticism, negative emotionality) is well documented (Nigg & Goldsmith, 1994). However, our knowledge of the genetic influence on BPD symptoms and features is rather limited.
Only two twin studies so far have provided data on BPD diagnoses and features. Torgersen (1984) reported a monozygotic (MZ) concordance rate of 0.0% and a dizygotic (DZ) concordance rate of 11.1% for BPD, suggesting that shared environmental factors influence the...