The biology of self-harm

Research about non-suicidal self-injury (NSSI) is still relatively new, but it is developing through different approaches such as the psychological, cultural, and more recently biological approach. Yet, it is still poorly understood from biological and clinical perspectives (Stanley, et al., 2010). These perspectives can be valuable for the understanding of self-harm. As Liu (2017) explains, self-reported data is not always accurate and there is a need for “laboratory tasks” to “clarify the mechanisms underlying NSSI”. A better biological understanding of self-harm could lead to the discovery of more effective interventions and treatments (Liu, 2017) such as pharmacological treatments (Stanley, et al., 2010). Findings, although often inconsistent, has been made about serotonin, the HPA axis, cortisol and endogenous opioids in relation to non-suicidal self-injury.


Serotonin – also known a 5-HT – is a hormone and neurotransmitter that has many functions. It has been found that diminished serotonin activity is associated with impulsive and aggressive behaviors, suicide attempts and depression (Roberts, 2003; Groschwitz & Plener, 2012).

Research has found a lower blood serotonin level in people with NSSI (Ashton, Marshall, Hassanyeh, Marsh, & Wright-Honari, 1994; Roberts, 2003). But findings on serotonin are inconsistent. According to Groschwitz & Plener (2012) “Serotonin is more related to aggressive or violent behaviors in general than to self-injurious behaviours in particular” and while the lack of serotonin can lead to impulsive behaviors, self-harm is often not impulsive.


The HPA axis plays a role in our behavioral and physiological response to stress. It helps us cope with stress and “recover from stressful experiences” (Kaes, et al., 2012). Experiencing stress results in an elevated secretion of cortisol (Groschwitz & Plener, 2012), which is often called the “stress hormone”.

Surprisingly, people who suffer from post-traumatic syndrome (PTSD), chronic stress or stress-related bodily disorders have a reduced cortisol secretion (Kaes, et al., 2012; Groschwitz & Plener, 2012). Kaes et al. (2012) suggests that this reduced cortisol secretion may be due to the prolonged activation of the HPA axis in people with chronic stress. It has also been found that the HPA axis is dysfunctional and hyporesponsive to acute stress in people with NSSI and that the secretion of cortisol is reduced as well (Stanley, et al., 2010; Kaes, et al., 2012; Groschwitz & Plener, 2012). One possible explanation could be that patients who engage in NSSI may experience chronic stress that alters their HPA (Kaes, et al., 2012).

This reduced secretion of cortisol in case of stress could “induce a more severe experience of stress and reduced recovery from stress” which could make people with NSSI more vulnerable to acute stress and may adopt unhealthy stress regulation strategies such as NSSI (Kaes, et al., 2012). Yet, it is still unclear whether the alterations in the HPA axis are a cause of NSSI or “just occur concomitantly (Kaes, et al., 2012).


Endogenous opioids are neurotransmitters that influence our perception of pain (Sher & Stanley, 2008; Stanley, et al., 2010). They have analgesic (Sandman & Hetrick, 1995; Roberts, 2003; Groschwitz & Plener, 2012; Liu, 2017), addictive (Groschwitz & Plener, 2012) and euphorigenic properties (Sandman & Hetrick, 1995; Pembroke, Shaw, & Thomas, 2007). The good feelings that we feel after eating chocolate, having an orgasm or after physical exercise could be caused by the release of endogenous opioids (Pembroke, Shaw, & Thomas, 2007). Beta-endorphin and met-enkephalin (two endogenous opioid peptides) are involved in stress-induced analgesia (Sher & Stanley, 2008; Stanley, et al., 2010).

Studies have found lower levels of endogenous opioids in people who self-harm repeatedly (Sher & Stanley, 2008; Groschwitz & Plener, 2012; Liu, 2017) but some research contradicts or questions this hypothesis (Pembroke, Shaw, & Thomas, 2007; Blasco-Fontecilla, et al., 2016). People with NSSI have low levels of beta-endorphin and enkephalins (Stanley, et al., 2010; Liu, 2017).

However it has been found that there is an increased secretion of beta-endorphin after an episode of self-harm (Sandman & Hetrick, 1995; Roberts, 2003; Liu, 2017). Therefore, the low level of endogenous opioids in self-harmers may be restored by engaging in NSSI (Stanley, et al., 2010; Groschwitz & Plener, 2012) as pain stimulates the release of opioids into the bloodstream (Sandman & Hetrick, 1995). Liu (2017) suggests that as the level of endogenous opioids in people with NSSI is habitually low, their effect could be felt more strongly when released by NSSI. So self-harm can be understood as a stimulus to release endogenous opioids and feel their euphorigenic properties in order to relieve psychological pain while not feeling too much physical pain as these opioids also have analgesic qualities.

We do not know however if these low levels existed before or are caused by self-harm (Stanley, et al., 2010; Kirtley, O’Carroll, & O’Connor, 2014; Liu, 2017). It could therefore be a predisposition or a result of self-harm. One possible explanation is that opioid deficiency could be caused by chronic and childhood stress or trauma (Sher & Stanley, 2008; Stanley, et al., 2010).


These findings should be interpreted carefully as studies are still inconsistent. Research faces several obstacles. First for ethical reasons, actual NSSI cannot be observed or analyzed so researchers need to rely on alternatives to replace self-harm. Moreover, most studies face methodological issues as peripheral measures are often used instead of cerebrospinal fluid (CSF). The analysis of these two fluids is not interchangeable and CSF is preferable but its sampling via lumbar puncture is seen as invasive, has side effects and can generate stress which may lead to altered results (Kirtley, O’Carroll, & O’Connor, 2014).

While a biological approach to NSSI can help us better understand this behavior, we must keep in mind that self-harm is not purely biological. Pembroke, Shaw & Thomas (2007) argues, that self-harm “occurs in times of great emotional distress, depression, and in response to circumstances and events. These are not biological incidents”. As Roberts (2003) explains, “it is impossible to separate the bio-psychosocial factors into discrete entities; they are closely linked and have mutual impact”. Some pharmacological treatments might “block the reward of enhanced endogenous opioids” and lead to the “extinction” of the self-injurious behavior (Sher & Stanley, 2008) but self-harm is a coping mechanism. If the individual is deprived of NSSI, he or she might not be able to cope with his or her suffering. Therefore, as Roberts (2003) points out, “[p]sychotropic medication should be used to augment, not replace, behavioral therapy”.


Ashton, C., Marshall, E., Hassanyeh, F., Marsh, V., & Wright-Honari, S. (1994, December). Biological correlates of deliberate self-harm behaviour: A study of electroencephalographic, biochemical and psychological variables in parasuicide. Acta Psychiatrica Scandinavica, 90(5), pp. 316-323.

Blasco-Fontecilla, H., Fernández-Fernández, R., Colino, L., Fajardo, L., Perteguer-Barrio, R., & de Leon, J. (2016). The Addictive Model of Self-Harming (Non-suicidal and Suicidal) Behavior. Frontiers in Psychiatry, 7(8).

Groschwitz, R. C., & Plener, P. L. (2012). The Neurobiology of Non-suicidal Self-injury (NSSI): A review. 3, pp. 24-32.

Kaes, M., Hille, M., Parzer, P., Maser-Gluth, C., Resch, F., & Brunner, R. (2012). Alterations in the neuroendocrinological stress response to acute psychosocial stress in adolescents engaging in nonsuicidal self-injury. Psychoneuroendocrinology(37), pp. 157-161.

Kirtley, O., O’Carroll, R., & O’Connor, R. (2014). The Role of Endogenous Opioids in Non-SuicidalSelf-Injurious Behavior: Methodological Challenges. Neuroscience and Biobehavioral Reviews.

Liu, R. T. (2017). Characterizing the course of non-suicidal self-injury: A cognitive neuroscience perspective. Neuroscience and Biobehavioral Reviews.

Pembroke, L., Shaw, C., & Thomas, P. (2007, May). Biological reductionism of self-harm. Mental Health Practice, pp. 16-17.

Roberts, N. (2003, August). Adolescent Self–Mutilatory Behavior: Psychopharmacological Treatment. Child and Adolescent Psychopharmacology News, 8(5), pp. 10-12.

Sandman, C. A., & Hetrick, W. P. (1995). Opiate Mechanisms in Self-Injury. Mental Retardation and Developmental Disabilities Research Reviews, 1(2), pp. 130-136.

Sher, L., & Stanley, B. H. (2008). The Role of Endogenous Opioids in the Pathophysiology of Self-Injurious and Suicidal Behavior. Archives of Suicide Research, 12(4), pp. 299-308.

Stanley, B., Sher, L., Wilson, S., Ekman, R., Huang, Y.-y., & Mann, J. J. (2010, July). Nonsuicidal Self-Injurious Behavior, Endogenous Opioids and Monoamine Neurotransmitters. J Affect Disord, 124(1-2), pp. 134-140.