Contents

• Diagnostic Overlap Between DID and BPD
• Dissociation as an Opioid-Mediated Protective Mechanism
• Ultra-Low-Dose Naltrexone and Internal Accessibility
• When Structural Dissociation Co-Occurs with BPD
• Why Transdermal Buprenorphine May Help
• Clinical Implications
• A Brief Anecdote
• References

Note: Plural system (often used as plural systems) is a term used by people who experience more than one distinct internal individual, identity, or self-state within a single body. These internal individuals—sometimes called parts, headmates, or system members—may differ in age, role, affect, or sense of self, and may be more or less aware of one another. Plural systems include people diagnosed with dissociative identity disorder (DID), other specified dissociative disorder (OSDD), or other dissociative conditions, as well as people who do not identify their plurality as a disorder.

Additionally, not everyone with a dissociative disorder identifies as plural. Some prefer strictly clinical language. Both perspectives are respected here, and terminology is used descriptively rather than prescriptively.

In this article, the term plural systems is used descriptively and respectfully, regardless of whether a person identifies their experience as clinical, non-clinical, or somewhere in between.

This piece is written for two audiences:

For people navigating these diagnoses:

• Those diagnosed with DID or OSDD who may not realize they also meet criteria for borderline personality disorder (BPD)
• Those diagnosed with BPD who may not realize they are living with structural dissociation

For clinicians: Those interested in novel, biologically informed approaches to treating severe affective instability and dissociation, including low-dose buprenorphine

Diagnostic Overlap Between DID and BPD

Even at the level of diagnostic criteria alone, DID and BPD share several core features: nonsuicidal self-injury, dissociation, identity disturbance, affective instability, and trauma-linked interpersonal dysregulation. This overlap is not incidental. It reflects shared underlying neurobiology, particularly involving the endogenous opioid system.^{1 2}

Dissociation is mediated in part by endorphins and endogenous opioids. During inescapable threat, opioid release blunts pain, dampens affect, and allows psychological distance from experience.^{1 2}

Dissociation is not a failure of regulation. It is a solution. It is a protective response that works extremely well under overwhelming conditions. An “overwhelming” condition does not necessarily mean extreme, obvious, or intentional abuse.

Early in life, the nervous system depends on consistent connection and regulation from others. Periods of emotional unavailability, misattunement, or chronic aloneness can exceed a young child’s capacity to cope, even when caregivers are doing their best. In these contexts, dissociation can emerge as an adaptive way for the nervous system to manage more than it can integrate at the time.

Many people with structural dissociation do not consciously experience themselves as dissociated. The dissociation is doing its job: keeping traumatic material compartmentalized, reducing conscious distress, and maintaining functional appearance.

As described in the DSM-5-TR:

Most individuals with non-possession-form dissociative identity disorder do not overtly display, or only subtly display, their discontinuity of identity, and only a minority present to clinical attention with discernible alternation of identities.³

This contributes to why DID and other dissociative disorders may be overlooked in clinical settings, particularly when dissociation presents as emotional numbing, shutdown, or identity diffusion rather than overt switching. Even when dissociative disorders are recognized, treatment approaches vary widely, and many clinicians report limited training in working with dissociative presentations.⁴

Dissociation as an Opioid-Mediated Protective Mechanism

Endogenous opioids appear to play a central role in maintaining dissociative barriers. Small changes in opioid tone can increase or decrease internal separation, which helps explain why highly dissociative systems are often exquisitely sensitive to pharmacologic interventions that affect opioid signaling. In clinical contexts described as “severe DID,” dosage differences as small as 2 milligrams per day of naltrexone have been reported to determine whether suicidal parts or self-states are accessible in therapy at all.⁵

This sensitivity has direct clinical implications. In individuals who cannot recall large portions of their life history, even modest opioid blockade may increase memory access and reduce dissociative separation—effects that may or may not be experienced as tolerable or welcome. In these cases, very small starting doses of naltrexone are recommended. As described by Ulrich Lanius, some patients find that even 0.1 mg of naltrexone is excessive, and that doses in the range of 10 micrograms are better tolerated early in treatment (11:20 timestamp).⁶

Ultra-Low-Dose Naltrexone and Internal Accessibility

When tolerated, subtle modulation of opioid tone with ultra-low-dose naltrexone (ULDN) has been reported to increase internal accessibility and communication.⁶ Clinically, this can mean that parts or self-states become more co-conscious, memories can be approached without immediate shutdown, and affect becomes tolerable rather than overwhelming. Improvements in attention, body awareness, affect tolerance, and self-regulation have been observed alongside reductions in depersonalization, amnesia, tonic immobility, and self-injurious behavior.⁶

This shift matters because many trauma-focused therapies rely on dual awareness and sufficient affect tolerance. EMDR, somatic therapies, and attachment-focused interventions require the capacity to remain present while processing traumatic material. When internal communication is severely restricted, these modalities may instead trigger further dissociation or crisis states. Subtle opioid modulation may widen the window of tolerance just enough to make other treatments possible.⁶

These effects are not universally comfortable. Reported adverse responses include sleep disturbance, increased anxiety or avoidance, transient fear or rage, headaches associated with accessing previously dissociated material, and temporary intensification of attachment needs.⁶ Such reactions are often dose-dependent and may improve with careful titration.

For some plural systems without prominent borderline traits, ULDN alone may be sufficient to support trauma-oriented therapies such as establishing internal safety, attachment repair, EMDR, and somatic approaches.⁵ It is worth noting that ULDN for dissociation is an off-label use, as are many applications of low-dose naltrexone across autoimmune, pain, and neurodevelopmental conditions.^{7 8}

When Structural Dissociation Co-Occurs with BPD

The picture becomes more complex when structural dissociation co-occurs with BPD. In these systems, increasing internal access may simultaneously increase exposure to intense affect. For some individuals, this can initially heighten anxiety, fear, or anger, particularly if baseline regulation is fragile.⁶ Careful titration and close clinical monitoring are therefore essential. In these cases, opioid stabilization alone may be insufficient; broader affect-regulation strategies may need to be supported concurrently.

In BPD, the nervous system is often under chronic extreme stress. Repeated trauma and affective dysregulation drive massive episodic endogenous opioid release. Over time, the brain appears to become tolerant to baseline opioid signaling, requiring extreme distress to re-activate the system. Converging evidence suggests that individuals with BPD may have chronically low baseline endogenous opioid signaling, with compensatory changes in opioid receptor availability, and that self-injury and extreme distress can acutely stimulate endogenous opioid release and function as regulatory mechanisms.⁹

At this point, behaviors commonly associated with BPD—nonsuicidal self-injury, high-risk or self-destructive behaviors, trauma reenactment, and chaotic attachment patterns—can be understood as attempts at neurochemical self-regulation. These behaviors reliably trigger endogenous opioid release.⁹ They are not attention-seeking; they are survival strategies in a system that cannot otherwise achieve regulation.

Why Transdermal Buprenorphine May Help

For extremely sensitive systems, a transdermal buprenorphine patch may offer stabilization that other approaches cannot.

The lowest available patch delivers 5 micrograms per hour continuously. Buprenorphine’s pharmacology is unusual. It is a partial μ-opioid receptor agonist, meaning it turns the receptor on enough to provide opioid signaling, but with a built-in ceiling that limits how strong that signal can become. At the same time, it binds tightly to the receptor, which reduces the ability of other opioids—including the body’s own endogenous opioids such as endorphins—to attach and produce large surges of activity.^{10 11}

In practical terms, this creates a steadier baseline rather than sharp spikes followed by crashes. Buprenorphine also blocks κ-opioid receptors, which are strongly implicated in dysphoria, despair, and suicidal ideation.^{10 12}

Together, these effects may stabilize opioid tone while reducing the extreme fluctuations that drive trauma reenactment and crisis-based regulation. Clinically, this may reduce trauma-seeking behavior, soften dissociative barriers without collapsing them, and widen the window of tolerance just enough for therapy to proceed.

Importantly, the delivery method matters. Transdermal buprenorphine is absorbed slowly, reaching peak plasma levels much later than buccal or sublingual formulations, and is designed to provide continuous low-dose exposure over a full week.¹³ This slower, steadier profile may be particularly relevant for highly opioid-sensitive dissociative systems, where rapid receptor engagement and peak-trough effects can be destabilizing.

Clinical Implications

This is not a claim that buprenorphine cures DID or BPD, or that it is an established first-line treatment. Rather, for a subset of highly traumatized, opioid-sensitive systems—particularly when BPD co-occurs with structural dissociation—pharmacological support of baseline opioid tone may reduce crisis-dependent regulation and establish sufficient capacity for psychotherapeutic work.

For ultra-low-dose naltrexone: Extreme dose sensitivity is common in highly dissociative systems. Some patients cannot tolerate 0.1 mg (100 micrograms), and starting doses as low as 10 micrograms are recommended.⁶ Even small dosage changes—as little as 2 mg per day—can dramatically shift which parts or self-states are accessible.⁵ Titrate slowly and collaboratively, monitoring for increased memory access, shifts in co-consciousness, or emergence of previously inaccessible material. Increased internal access may temporarily heighten anxiety, sleep disturbance, intensified attachment needs, or affective dysregulation.⁶ This may be particularly true in systems where structural dissociation co-occurs with prominent borderline traits. These effects reflect the removal of dissociative barriers rather than direct stabilization.

For buprenorphine: The lowest-dose transdermal patch (5 mcg/hour, applied weekly) provides steady-state delivery with minimal peak-trough fluctuation,¹³ which may be better tolerated than sublingual formulations in highly dissociative systems. Unlike naltrexone, buprenorphine supplies baseline opioid tone rather than removing it, which may create a more supportive foundation—reducing dissociative fragmentation while maintaining internal cohesion. Expected outcomes include greater co-consciousness between parts, reduced compulsive dissociation, less reliance on crisis states for regulation, and improved capacity to engage with trauma-focused therapies.

For clinicians, if a patient reports marked sensitivity to opioid modulation or benefit from ultra-low-dose naltrexone, it is reasonable to hypothesize that dissociation is being pharmacologically mediated. In such cases, a continuously delivered buprenorphine approach may provide steadier baseline regulation than episodic modulation with naltrexone.

For patients, recognizing this mechanism can be unsettling. Dissociation hides itself by design. Understanding how the system regulates does not remove protection—it opens the possibility of safer, less costly ways to remain regulated and connected.

A Brief Anecdote

I want to end on one brief anecdote, offered not as evidence but as a signal. A close friend of mine with diagnoses of BPD, fibromyalgia, and self-diagnosed DID or OSDD, sought pain management after hearing that I had experienced significant relief from my own BPD symptoms using low-dose buprenorphine. She was prescribed a transdermal buprenorphine patch as part of her pain regimen; her dissociative and borderline diagnoses were not discussed in that context and are not listed on her chart, as doing so would likely have derailed the conversation.

The patch provided meaningful pain relief alongside her existing treatments. It was also associated with reduced dissociation, greater overall emotional stability, and most notably, the complete resolution of the suicidal depression she had been experiencing as part of her BPD.

This is an N=1 experience, not a claim of efficacy or universal response, but it made me hopeful. I share it in that spirit, in case it offers a small amount of hope to readers navigating similar terrain.

References