Aetiological pathways to Borderline Personality Disorder symptoms in early adolescence: childhood dysregulated behaviour, maladaptive parenting and bully victimisation

Abstract

Developmental theories for the aetiology of Borderline Personality Disorder (BPD) suggest that both individual features (e.g., childhood dysregulated behaviour) and negative environmental experiences (e.g., maladaptive parenting, peer victimisation) may lead to the development of BPD symptoms during adolescence. Few prospective studies have examined potential aetiological pathways involving these two factors. We addressed this gap in the literature using data from the Avon Longitudinal Study of Parents and Children (ALSPAC). We assessed mother-reported childhood dysregulated behaviour at 4, 7 and 8 years using the Strengths and Difficulties Questionnaire (SDQ); maladaptive parenting (maternal hitting, punishment, and hostility) at 8 to 9 years; and bully victimisation (child and mother report) at 8, 9 and 10 years. BPD symptoms were assessed at 11 years using the UK Childhood Interview for DSM-IV BPD. Control variables included adolescent depression (assessed with the Short Moods and Feelings Questionnaire-SMFQ) and psychotic symptoms (assessed with the Psychosis-Like Symptoms Interview-PLIKS) at 11 to 14 years, and mother’s exposure to family adversity during pregnancy (assessed with the Family Adversity Scale-FAI). In unadjusted logistic regression analyses, childhood dysregulated behaviour and all environmental risk factors (i.e., family adversity, maladaptive parenting, and bully victimisation) were significantly associated with BPD symptoms at 11 years. Within structural equation modelling controlling for all associations simultaneously, family adversity and male sex significantly predicted dysregulated behaviour across childhood, while bully victimisation significantly predicted BPD, depression, and psychotic symptoms. Children displaying dysregulated behaviour across childhood were significantly more likely to experience maladaptive parenting (β = 0.075, p < 0.001) and bully victimisation (β = 0.327, p < 0.001). Further, there was a significant indirect association between childhood dysregulated behaviour and BPD symptoms via an increased risk of bullying (β = 0.097, p < 0.001). While significant indirect associations between dysregulated behaviour, bully victimisation and depression (β = 0.063, p < 0.001) and psychotic (β = 0.074, p < 0.001) outcomes were also observed, the indirect association was significantly stronger for the BPD outcome (BPD – depression = 0.034, p < 0.01; BPD – psychotic symptoms = 0.023, p < 0.01). Childhood dysregulated behaviour is associated with BPD in early adolescence via an increased risk of bully victimisation. This suggests that childhood dysregulation may influence the risk of bully victimisation, which in turn influences the development of BPD. Effective interventions should target dysregulated behaviour early on to reduce exposure to environmental risks and the subsequent development of BPD.

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