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Introduction: Childhood ADHD, especially when persistent, is associated with the development of personality disorders, most notably borderline personality disorder (BPD; Matthiews & Philipsen, 2016). Among adult women with BPD, estimates of ADHD in childhood (41.5%) and adulthood (16.1%) are particularly striking. Recent evidence reveals that ADHD and BPD share common developmental pathways and commonly co-occur. Comorbid ADHD/BPD is associated with poor clinical outcomes, yet limited research exists on mechanisms of risk (e.g. childhood trauma) and intervention specific to this population (Calvo et al., 2020). Furthermore, most studies examine retrospective self-report of childhood ADHD in male-dominated samples. Examination of BPD in prospective, longitudinal studies of females with ADHD is crucial. Given the high rates of self-harm among females with ADHD, examining these transdiagnostic symptoms and linkages to BPD across development is critical. We seek to fill this gap by prospectively examining (1) whether and how ADHD symptoms in childhood, and persistence of ADHD symptoms into adulthood, increase risk for BPD in adulthood among females, and (2) theory-informed mediators of this relation.
Method: Participants comprised an ethnically diverse sample of females (47% non-white) with (n = 140) and without (n = 88) childhood-diagnosed ADHD, who were prospectively followed across 16 years. In childhood (Mage = 9.6), ADHD hyperactive-impulsive (HI) and inattentive (IA) symptoms were assessed by teacher- and parent-report. In late adolescence (Mage = 19.6), NSSI severity was assessed by the Self-Injury Questionnaire. In young adulthood (Mage = 25.6), ADHD persistence was assessed by multiple informants; childhood trauma was assessed by the ACE Questionnaire; DSM-IV TR criteria for BPD were assessed by the SCID-II. Covariates included age, race, and SES.
Results: Of the 17 females who met criteria for BPD in young adulthood, 13 (76%) had childhood ADHD, in particular the ADHD-Combined presentation (both HI and IA symptoms; 59%). Logistic regression revealed that severity of HI, but not IA, in childhood predicted meeting criteria for BPD in young adulthood (OR = 1.95, CI95=[1.11-3.51]). When adjusting for IA symptoms, age, race, and SES, however, this result was no longer significant. ADHD persistence from childhood through young adulthood was significantly associated with meeting criteria for BPD in young adulthood (OR = 5.02, CI95=[1.60-19.05]). Bootstrapped mediations revealed that both NSSI severity (IE=0.0413, SE=0.0162, CI95=[0.0134, 0.0754]) and childhood trauma history (IE=0.0247, SE=0.0107, CI95=[0.0069, 0.0476]) significantly mediated the relation between childhood HI symptoms and young adult BPD.
Discussion: Findings suggest that females with childhood-diagnosed ADHD are at increased risk for the development of BPD by adulthood. Females with persistent ADHD are at particularly high risk for comorbid BPD. Both NSSI severity by late adolescence and a history of childhood trauma helped to explain the link between childhood ADHD and young-adult BPD, consistent with a biosocial developmental model of BPD. However, the directionality of NSSI severity is questionable, as some females may have already met criteria for BPD in adolescence. Further research is needed in prospectively identifying developmental mechanisms of risk for BPD in individuals with ADHD, especially females, to inform early intervention.