bpd.fyi
A patient-run resource on buprenorphine, BPD, and the endogenous opioid system.
Welcome
Many people with Borderline Personality Disorder continue to struggle with emotional pain and suicidal thoughts even after trying standard treatments.
A few years ago, I kept running into research linking BPD to the endogenous opioid system, and eventually to early evidence that low-dose buprenorphine might help. Even though it’s normally prescribed for opioid use disorder, very low doses reduced the emotional pain and instability that made daily life hard for me, and my suicidal thoughts resolved completely once I started treatment.
I built this page to share the research and my experience in case it helps someone else.
How Buprenorphine Works
Our brains have an endogenous opioid system that helps regulate physical pain, emotional pain, attachment, and distress. In BPD, several researchers have proposed that this system becomes dysregulated, often as a result of chronic invalidation, trauma, or ongoing inflammation.
Buprenorphine is unique because it:
- Partially activates the mu-opioid receptor — reduces emotional and physical pain and supports social connection/seeking behavior
- Blocks the kappa-opioid receptor — reduces dysphoria, stress-driven distress, and the aversive emotional pain response
It’s the only prescription medication that combines mu-agonism with kappa-antagonism.
Because buprenorphine is an opioid, people sometimes worry about addiction. At the very low doses studied for BPD and chronic suicidality, the addiction risk appears to be significantly lower than with full-agonist opioids, but physical dependence can still occur with long-term use. For people with a history of opioid addiction, this is an important consideration to discuss with a clinician. Many trials described their use as “time-limited,” partly because long-term data is still limited.
Other compounds with overlapping mechanisms:
- Low-dose naltrexone (LDN, 0.5–4.5 mg) — at low doses, naltrexone briefly blocks opioid receptors and then appears to increase endogenous opioid activity and reduce inflammation after it wears off. This is different from the standard 50 mg dose typically used for addiction or alcohol use disorder, which produces full opioid blockade. Naltrexone is not an opioid, and LDN does not carry a risk of opioid addiction.
- Kratom — a plant whose active alkaloids act as mu-opioid agonists with some kappa-opioid antagonism. It is much weaker and shorter-acting than buprenorphine, so people often need higher and more frequent doses to get similar effects. Kratom can be addictive and may cause dependence and withdrawal, and product quality and dosing are highly variable.
I'm sharing this information for context, not as a recommendation. LDN gave me some benefit, mostly improved sleep and a small lift in mood, but it didn’t address the social connection and emotional regulation problems that made daily life difficult. Some people also experiment with kratom because it has similar receptor activity, but it carries real risks. For my own BPD symptoms, prescribed low-dose buprenorphine has been far more effective and predictable than anything over-the-counter.
Medication is highly individual. Please research carefully and talk with a clinician.
My Experience
Low-dose buprenorphine made a noticeable difference for me. I took it long-term, and the stability lasted. I later paused treatment to see if I could manage symptoms through strict diet and inflammation control, which was possible but very limiting, so I chose to restart it.
- My emotions became manageable
- My relationships stabilized
- The chronic emptiness lifted
- Suicidal thoughts disappeared
My doctor started me at 0.5 mg, which ended up being too much — I had nausea and confusion. Lowering the dose resolved the side effects completely. To measure tiny amounts accurately, I diluted a 2 mg tablet in 2 mL of distilled water and used a 1 mL oral syringe to draw small measured doses from that.
DBT gave me the tools to manage intense distress, but it didn’t change the cycles of suicidal ideation. Buprenorphine was the first treatment that ended those cycles and allowed my nervous system to calm down.
Research & Background
Key papers on buprenorphine for BPD or treatment-resistant depression:
-
The Interpersonal Dimension of Borderline Personality Disorder: Toward a Neuropeptide Model (2010)
Proposes that many BPD symptoms stem from dysregulation in the brain’s endogenous opioid system, and suggests that buprenorphine could be therapeutic because of its partial opioid-agonist effects. -
Safety, Tolerability, and Clinical Effect of Low-Dose Buprenorphine for Treatment-Resistant Depression (2014)
Shows low doses improve mood in people whose depression didn’t respond to standard treatments. -
Ultra-Low-Dose Buprenorphine for Severe Suicidal Ideation (2015)
Finds a rapid and clinically significant reduction in suicidal thinking, often within the first week. (Some patients improved within several days.) -
Use of Buprenorphine in Treatment of Refractory Depression — A Review (2017)
Summarizes evidence supporting buprenorphine’s antidepressant and anti-suicidal effects. -
The Use of Buprenorphine/Naloxone to Treat Borderline Personality Disorder: A Case Report (2022)
Documents successful treatment of BPD symptoms using buprenorphine/naloxone. The patient started at 2 mg and titrated up to 8 mg, which is higher than the doses used in low-dose studies but was effective for this individual case.
Most low-dose buprenorphine studies used doses in the range of 0.1–0.44 mg per day. These microdoses are far smaller than the doses used for opioid use disorder, and the clinical effects in BPD and chronic suicidality appear to come from partial mu-agonism at very low levels. My own effective dose fell in this range as well.
Another important paper is Borderline Personality Disorder: A Dysregulation of the Endogenous Opioid System? (2010). Seeing a biological explanation for BPD that matched my lived experience helped me understand my symptoms in a way that finally made sense.
Access to Research
Full-text papers aren’t always freely available. Tools like Sci-Hub and other publicly available mirrors exist, and many people use a DOI or article title to look up papers directly.
Access to medical information shouldn’t be gatekept. For many people, being able to read the research directly is the difference between suffering without answers and finding something that works.