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The developmental precursors of borderline personality disorder symptoms at 11 years in a British cohort

Borderline Personality Disorder (BPD) is a severe and chronic mental health disorder, affecting many areas of functioning including: affect regulation, impulse control, interpersonal relationships and self-image. Causal factors are only partly known due to a scarcity of prospective, longitudinal studies which enable one to delineate the time ordering of antecedents, and allow for tentative causal inferences. This thesis explored the developmental precursors of BPD symptoms at 11 years, using a British cohort sample, with assessments pertaining to the study child from pregnancy to 11 years of age. Three studies were conducted. Firstly, the predictive relationship between exposure to maladaptive parenting and subsequent BPD symptoms was explored within a child population, using a clinically relevant assessment of BPD symptoms. This association has been previously shown in a range of retrospective studies. Secondly, the role of peer victimisation in the development of BPD was considered. This study was designed to extend current aetiological models, which focus on parental rather than peer relationships. It was based on the recognition of a strong interpersonal core in the BPD symptom constellation, and the role of trauma experiences in the development of BPD. Finally, the third study was designed to consider how these two experiential factors (maladaptive parenting and peer victimisation) might magnify a predisposition towards dysregulation, eventually culminating in BPD symptoms. Data was obtained from the Avon Longitudinal Study of Parents and Children (ALSPAC), which studied 6,050 children (43.1% of the total sample population), using questionnaire and interview assessments. Results revealed that, firstly, family adversity during pregnancy and suboptimal parenting, during early to middle childhood was predictive of BPD symptoms at 11 years. Secondly, peer victimisation during early to late childhood was predictive of BPD symptoms at 11 years. There was an especially strong dose response effect for severe, combined or chronic victimisation. Finally, those evincing stable dysregulated trait behaviour from 4 to 8 years were more likely to develop BPD symptoms, and this effect was especially strong for high levels of dysregulation. Consistent with the biosocial developmental model of BPD, the association was fully mediated by psychosocial risk factors (peer victimisation). Those with high levels of dysregulation were more likely to be victimised and, in turn, develop BPD symptoms. Further, the indirect associations were significantly stronger for BPD, compared to psychotic or depression outcomes. The strengths and weaknesses, along with practical and theoretical implications, and future directions are discussed in the final chapter.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:560345
Date January 2012
CreatorsWinsper, Catherine
PublisherUniversity of Warwick
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Sourcehttp://wrap.warwick.ac.uk/49638/

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