New research uncovers a possible cause of borderline personality disorder

Nov 16, 2020

Borderline personality disorder (BPD) is a mental health condition that impacts the way you think and feel about yourself and others, causing problems in everyday functioning. It includes self-image issues, difficulty managing emotions and behavior, self-harming behavior, and a pattern of unstable relationships. Using brain imaging Dr. Nathan Kolla has found evidence that an elevated amount of a chemical called FAAH may be linked to BPD, raising the possibility that existing medications could help treat the disorder.

We spoke to Dr. Kolla and the methods he used, his findings, and the potential impact his research could have on those living with BPD.

What is a [11C]CURB Positron Emission Tomography​ (PET) scan, and how was it used for this research?

NK: A PET scan is a brain imaging technique. A radiotracer is injected into a vein and travels to the brain, where it gives off a small amount of energy in the form of photons. These rays can then be located and tracked as they move within the brain. [11C] CURB is a radiotracer that attaches to a brain chemical called fatty acid amide hydrolase (FAAH), and the brain pictures will show brain areas where FAAH level is highest.

What motivated this research?

NK: I have always been curious about the brain chemistry of different forensic psychiatric populations, like those with personality disorders who show high levels of aggression and impulsivity. I am motivated to learn more about the brain chemistry in order to pave the way for new drug treatments that could effectively treat these conditions. Forensic psychiatric populations are very understudied and could highly benefit from more brain research.

What was the most important finding of this study, in your opinion?

NK: We found that levels of the brain chemical FAAH were higher in certain brain areas of borderline personality disorder (BPD) compared with healthy volunteers. This is the first finding of higher brain FAAH levels for any psychiatric condition. FAAH brain levels were also related to greater anger and hostility in BPD. It is possible that lowering FAAH levels in these brain regions could relate to improvements in anger, hostility, and other symptoms of BPD.

How does this change treatment in patients with borderline personality disorder?

NK: We know that the mainstay of treatment for BPD is talk therapy. However, talk therapy is expensive, not always easy to access, and can take a long time to work. Medications are also important in the treatment of BPD and most patients with BPD take several medications. However, there is no single medication approved by Health Canada for the treatment of BPD. Notably, medications that lower brain FAAH levels are being tested for other psychiatric disorders. If other researchers similarly found that brain FAAH levels were higher in BPD, this would provide a strong incentive for testing FAAH blockers in clinical trials as potential new treatments for BPD.

Any next steps?

NK: Because abnormal FAAH levels have been implicated in many psychiatric disorders, we are also using PET scans to study FAAH levels in major depressive disorder alone as well as major depressive disorder in combination with BPD. We believe that brain FAAH levels will be higher in both groups.

What is the major take home message for the public?

Although there are no Health Canada-approved medications for BPD, most patients are still prescribed them. We have shown that brain FAAH levels are higher in BPD, and there are currently treatments that can block FAAH. We hope that our results can lead to new scientifically tested treatments, such as FAAH blockers, that will prove useful to help manage BPD.

ImPACT Committee includes Krista Lanctôt, Alastair Flint, Meng-Chuan Lai and Simone Vigod.

Kolla, N. J., Mizrahi, R., Karas, K., Wang, C., Bagby, R. M., Mcmain, S., . . . Boileau, I. (2020). Elevated fatty acid amide hydrolase in the prefrontal cortex of borderline personality disorder: A [11C]CURB positron emission tomography study. Neuropsychopharmacology, 45(11), 1834-1841. doi:10.1038/s41386-020-0731-y

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