The role of endogenous opioids and monoamine neurotransmitters in non-suicidal self-injury
Leo Sher, M.D.
Our research work, “Non-suicidal self-injurious behavior, endogenous opioids and monoamine neurotransmitters” was published 10 years ago in the July 2010 issue of the Journal of Affective Disorders (1). The objective of the study was to examine the role of endogenous opioids and monoamine neurotransmitters in non-suicidal self-injury (NSSI).
We compared cerebrospinal fluid (CSF) levels of endogenous opioids, 5-hydroxyindolacetic acid (5-HIAA) and homovanillic acid (HVA) in individuals with a history of repeated NSSI with a diagnostically-matched group of people who had never engaged in non-suicidal self-injury (no NSSI). History of suicidal behavior, demographic parameters, and psychopathology was assessed. All patients were diagnosed with a Cluster B personality disorder (i.e., borderline, antisocial, narcissistic or histrionic) (N=29) and had a history of at least one suicide attempt. Fourteen participants had a history of repeated NSSI in adulthood and 15 did not. The mean age of the sample was 35.5 ± 9.1 (range 18-65). CSF samples were collected via lumbar puncture, and concentrations of β-endorphin, met-enkephalin, dynorphin, the serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and the dopamine metabolite, homovanillic acid (HVA), were determined for all participants.
The NSSI and no NSSI groups did not differ with respect to background characteristics: age, sex, ethnicity, marital status, religious affiliation, education level, or employment rate. Severity of depression, hopelessness and overall psychopathology was greater in the NSSI group. The NSSI group had significantly lower levels of CSF beta-endorphin and met-enkephalin when compared with the no NSSI group. CSF dynorphin, HVA and 5-HIAA levels did not differ.
Based on our findings, we proposed a model of non-suicidal self-injury. According to our model, opioid deficiency could result from chronic and severe childhood stress and trauma, such as abuse, neglect and loss or from a biological predisposition. Because endogenous opioids play a role in pain threshold and perception, they are likely candidates for involvement in NSSI, a behavior frequently associated with the need to feel pain or relieve emotional tension. Traumatized individuals may need increased levels of endorphins to cope with stress, and NSSI may be an effort at increasing the endogenous opioids to restore homeostasis.
If the endogenous opioid system is central to repetitive self-injury, then treatment with a long-acting opioid antagonist could block the reward of enhanced endogenous opioids caused by such behaviors and subsequently lead to their extinction. Therefore, drugs acting on the opioid system warrant exploration as pharmacological treatments for NSSI.
- Stanley B, Sher L, Wilson S, Ekman R, Huang YY, Mann JJ. Non-suicidal self-injurious behavior, endogenous opioids and monoamine neurotransmitters. J Affect Disord. 2010 Jul;124(1-2):134-40. doi: 10.1016/j.jad.2009.10.028. Epub 2009 Nov 25.