Near the end of a 2019 talk on low-dose naltrexone, Lanius remarked of trauma patients: “They’re addicted to their own opioids.”¹

He was referring to endogenous opioids, the body’s internally produced pain- and stress-regulating neurochemicals. In some individuals with dissociative disorders, trauma reenactment and intense, self-destructive behaviors may stimulate this endogenous opioid system. The behaviors are maladaptive, but the underlying mechanism may be regulatory, as the nervous system seeks relief.

If trauma-related dysregulation involves instability in endogenous opioid tone, the overlap between borderline personality disorder (BPD) and substance use disorders deserves closer examination.

Up to 75% of individuals with BPD will meet criteria for substance use disorder in their lifetime. Alcohol, opioids, and benzodiazepines are frequently reported substances in this population, and all directly or indirectly interact with the opioid system.² Conversely, in one outpatient sample of patients initiating buprenorphine for opioid addiction, nearly 44% exceeded the screening cut-off for borderline personality features.³ This degree of overlap suggests shared biological vulnerability.

BPD is frequently framed as a disorder of behavior or motivation. Yet if endogenous opioid dysregulation contributes to affective instability, chronic emptiness, self-injury, and interpersonal crises, these behaviors may represent attempts at neurobiological self-regulation rather than willful noncompliance.²

Some authors have proposed that substance use in BPD may partially reflect attempts to modulate distressing internal states. In opioid use disorder (OUD) treatment settings, case-level reports have described patients preferring to remain on low-dose buprenorphine maintenance because they subjectively feel “normal.”⁴ While such observations do not establish mechanism or indication, they suggest that buprenorphine’s effects may extend beyond withdrawal suppression or craving reduction in a subset of patients.

Full opioid agonists carry escalating tolerance and overdose risk. Buprenorphine, as a partial agonist with a ceiling effect on respiratory depression, presents a different pharmacologic profile and has demonstrated mortality-reducing effects in OUD populations.⁵

This raises a clinical and public health question worth investigating:

If a subset of individuals with BPD have underlying opioid-system dysregulation, could carefully studied, low-dose buprenorphine intervention improve regulation capacity and reduce progression to high-risk opioid exposure?

Recent legislative changes in the United States have eased restrictions on buprenorphine prescribing. As access expands, there is an opportunity not only to treat OUD, but to consider whether earlier, regulation-focused interventions could reduce vulnerability in high-risk populations.

Reframing BPD through a regulation-first lens does not negate the importance of psychotherapy, skills training, or trauma-informed care. Rather, it recognizes that the ability to use skills depends in part on biological regulatory capacity.

If opioid-system dysregulation is contributing to both BPD symptom expression and opioid vulnerability, prevention efforts may need to begin before the first overdose.

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