Stress Reactivity in Borderline Personality Disorder

Open Access
Graduate Program:
Doctor of Philosophy
Document Type:
Date of Defense:
October 28, 2010
Committee Members:
  • Kenneth Levy, Dissertation Advisor
  • Kenneth Levy, Committee Chair
  • Aaron Lee Pincus, Committee Member
  • Reginald Adams Jr., Committee Member
  • Douglas A Granger, Committee Member
  • emotional dysregulation
  • emotion
  • stress
  • alpha-amylase
  • cortisol
  • borderline personality disorder
  • HPA axis
  • autonomic
  • affect
  • reactivity
Emotional dysregulation is seen by many clinicians and researchers as a core feature of borderline personality disorder (BPD). However, studies of emotional reactivity among individuals with BPD have yielded mixed findings, leaving uncertainty regarding the nature of emotional dysregulation in BPD. The current study examined neuroendocrine, autonomic, and subjective emotional reactivity in response to a social stress paradigm (the Trier Social Stress Test; Kirschbaum, Pirke, & Hellhammer, 1993) in 33 women with BPD as compared to two psychologically healthy comparison groups: 27 women who scored similarly to the BPD group on measures of trait negative affect and impulsivity (temperamentally-matched controls (TMCs)); and 30 women who scored in the average range on these traits (non-temperamentally-matched controls (NTMCs)). Repeated saliva samples were taken at eight time points and assayed for salivary cortisol and alpha-amylase (sAA). In addition, subjective stress response and changes in negative affect were measured through self-report instruments. It was hypothesized that the BPD group, in comparison to both control groups, would demonstrate greater cortisol, sAA, and subjective negative affective reactivity and impaired recovery to baseline levels after stress. Contrary to the hypotheses, the results suggested neuroendocrine and autonomic hyporeactivity accompanied by high general negative affectivity in those with BPD. Specifically, the BPD group demonstrated attenuated cortisol and sAA reactivity to the stressor as compared to both comparison groups. Although the BPD group reported more negative affect overall across the experiment than both comparison groups, there was only a marginally significant difference between the NTMC and BPD groups in post-stress negative affect when controlling for pre-stress negative affect. In addition, both the BPD and TMC groups reported experiencing the procedure as more stressful than the NTMC group. BPD patients who reported higher levels of childhood trauma tended to have higher baseline sAA, less sAA reactivity, and a trend toward higher overall sAA output, in comparison to both healthy controls and BPD patients who reported less severe childhood trauma. These results add to the emerging body of literature suggesting extreme negative affectivity, but not necessarily hyperreactivity, of emotional responses in those with BPD. Moreover, the attenuated cortisol and sAA reactivity in the BPD group suggests dysregulation of the stress response system in these patients that manifests in hyporeactivity, rather than hyperreactivity, at the level of glucocorticoid and central noradrenergic output in response to stress. The differences between the BPD and TMC groups in most indices of emotional response suggest that trait negative affect and impulsivity cannot fully explain extreme negative affectivity or neuroendocrine abnormalities in patients with BPD.