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In a review article published in the American Journal of Psychiatry, Barbara Stanley and Lawrence Siever introduce a new, cogent, and reasonably comprehensive neurobiological model of borderline personality disorder (BPD). This model links self-injurious behavior and interpersonal difficulties in BPD patients to neuropeptide activity. The researchers argue that dysregulated opioid, oxytocin, and vasopressin neuropeptide systems contribute to behavioral and affective dysfunction and interpersonal problems for individuals with BPD. The model is comprehensive in that it also aims to elucidate the unstable relationships, feelings of emptiness, and other experiences of patients with BPD.
Many studies have documented the involvement of endogenous opioids in mediating physical and emotional pain. Stanley and Siever posit that opioids also play a role in the experience of negative emotions and self-injurious behavior, which are common features of BPD. Support for this hypothesis comes from studies demonstrating low baseline opioid levels in limbic circuitry (e.g., cingulate cortex and amygdala) and increased opioid receptors throughout the brain in individuals with BPD. The authors propose that altered opioid functioning may relate to the chronic mental pain, lack of a sense of well-being, sensitivity to rejection, and difficulties in self-soothing that are associated with BPD. Specifically, opioid release