Non-Suicidal Self-Injury: Aetiology

This article reviews the psychological, social, and neurobiological factors which tend to generate and maintain non-suicidal self-injury (NSSI).

Related articles: Non-Suicidal Self-Injury: Context, Forms and Functions, Non-Suicidal Self-Injury: Prevalence, Risk and Protective Factors.

Introduction

In previous articles, we discussed the forms and function of non-suicidal self-injury, or NSSI (first article), and the prevalence, risk and protective factors, and warning signs that self-harm may be occurring (second article). Today we investigate how NSSI may get started in the first place, asking: what kinds of factors in a person’s life tend to draw them into self-injuring as a coping solution? The factors span psychological, social, and neurobiological domains. First up are the psychological factors.

Psychological dynamics of NSSI

This aetiological domain encompasses both affect and cognition and also interpersonal/developmental impacts.

Emotion regulation and relief

A large body of work situates NSSI within difficulties identifying, tolerating, and modulating emotion. Laboratory and self-report data indicate that NSSI can rapidly reduce high arousal negative affect (e.g., physiological tension, anger), which negatively reinforces the behaviour and promotes habit learning over time. Meta-analytic and conceptual reviews consistently link emotion dysregulation to NSSI and outline specific regulatory “families” (situation selection, attentional deployment, cognitive change, response modulation) through which NSSI may operate (Wolff et al, 2019; McKenzie & Gross, 2019).

Cognitive-affective vulnerabilities

Several transdiagnostic factors are implicated. Self-criticism and diminished aversion to NSSI cues have emerging support as risk processes; both may lower the threshold to engage in NSSI during affective spikes. Alexithymia—difficulty identifying and describing feelings—is robustly associated with NSSI and likely contributes via poor emotion labelling and planning of adaptive coping (Fox et al, 2018; Greene et al, 2020).

Interpersonal and developmental context

Interpersonal functions (e.g., signalling distress, reducing conflict, obtaining support) are part of the functional repertoire (i.e., how self-harm is utilised) for many, particularly in invalidating environments. Developmentally, adversity—including childhood maltreatment—elevates risk; meta-analyses show that sexual, physical, and emotional abuse and neglect are each associated with higher odds of NSSI. These experiences may contribute to emotion-regulation deficits, hyperarousal, and interpersonal mistrust that make NSSI more likely when stress peaks (Klonsky, 2007; Schmaal & Bendall, 2018).

Escalation and risk coupling with suicidality

Although defined by the absence of intent to die, NSSI meaningfully increases future suicide risk. Meta-analytic evidence indicates that a history of NSSI is among the strongest predictors of subsequent suicide attempts (odds ratios ≈4), and within self-injuring samples, suicide attempt history is most strongly associated with current suicidal ideation, greater NSSI frequency, use of multiple methods, and hopelessness. Clinically, repeated NSSI may lower fear of pain/injury and increase capability for suicide, a mechanism emphasised in contemporary suicide theories (Ribeiro et al, 2016; Victor & Klonsky, 2014).

Psychiatric comorbidity with NSSI

Not surprisingly, numerous mental health conditions frequently co-occur with self-harm.

Depression and anxiety (emotional disorders)

A rigorous meta-analysis shows medium-to-large associations between NSSI and mood/anxiety disorders overall, suggesting shared vulnerabilities in negative affectivity and regulation (e.g., rumination, avoidance). Clinically, depressive episodes often co-occur with spikes in NSSI urges. Anxiety (including social anxiety and generalised anxiety) is likewise common (Bentley et al, 2015).

Borderline personality disorder (BPD)

Among categorical diagnoses, BPD shows the most pronounced and clinically salient comorbidity with NSSI. NSSI is one of the DSM indicators of BPD and is frequently used to regulate intense, rapidly shifting affect and to manage feelings of emptiness or self-directed anger. Network and review studies in adolescents and adults underscore tight coupling between BPD symptoms (e.g., affective instability, identity disturbance) and NSSI behaviour (Reichl & Kaess, 2021; Buelens et al, 2020).

Eating disorders (EDs)

Comorbidity between eating disorders and NSSI is substantial. A meta-analysis in Psychological Medicine reported that about 27% of individuals with EDs have a lifetime history of NSSI, with higher rates in bulimia nervosa than anorexia nervosa—consistent with transdiagnostic traits (perfectionism, self-criticism, impulsivity) and shared regulatory functions (e.g., relief from aversive affect via body-focused acts). Co-occurrence is associated with greater clinical severity and suicide risk (Cucchi et al, 2016).

Post-traumatic stress disorder (PTSD) and trauma exposure

PTSD symptoms—particularly hyperarousal and intrusive re-experiencing—are associated with NSSI, and individuals with trauma histories have elevated risk across maltreatment subtypes. Meta-analytic work in The Lancet Psychiatry confirms positive associations between all five maltreatment subtypes and NSSI, highlighting trauma-informed formulation as standard practice when NSSI is present (Alharbi et al, 2020; Schmaal & Bendall, 2018).

Externalising problems and substance use

Beyond “emotional disorders,” meta-analytic evidence identifies externalising symptoms (aggression, conduct problems), impulsivity, and personality pathology such as found in Cluster B of the DSM (i.e., the antisocial, histrionic, borderline, and narcissistic personality disorders) as correlates or risk factors for NSSI. Substance misuse often co-occurs and can both precipitate and be reinforced by NSSI via disinhibition and maladaptive coping cycles (Fox et al, 2015).

Integrative picture

Taken together, the evidence supports a multi-level, transdiagnostic account: distal vulnerabilities (e.g., maltreatment, temperament, alexithymia, self-criticism) shape emotion-processing and interpersonal schemas. Proximal triggers (e.g., conflict, rejection, intense shame/anger, dissociation) generate aversive arousal. NSSI then functions—often powerfully—as a rapid, reliably effective (but short-lived) regulator of internal states and sometimes of social environments.

Learning mechanisms (negative and positive reinforcement) drive repetition and, for some, escalation (more frequent acts, more methods), which in turn increases suicide capability and attempt risk, even though the immediate motives are typically non-suicidal. This framework aligns with the Four-Factor Model (discussed in the first article of this series) and contemporary transdiagnostic models and explains the broad comorbidity profile observed across mood, anxiety, personality, eating, and trauma-related disorders (Bentley, Nock, & Barlow, 2014); Bentley et al, 2015).

Clinical implications

What may we take away from these robust findings regarding the psychological dynamics and co-morbidity of psychological factors with self-harm? They point to three primary implications for clinicians. We need to:

1. Assess functions, not just frequency. Functional assessment tools (e.g., the Inventory of Statements About Self-Injury, or ISAS) help identify an individual’s dominant intrapersonal and interpersonal reinforcers, which guides targeted intervention (Klonsky & Glenn, 2009).
2. Screen systematically for comorbidity. Given robust links with depressive/anxiety disorders, BPD features, EDs, PTSD, externalising symptoms, and substance use, routine assessment for these conditions is warranted. Comorbidity often maintains NSSI unless addressed directly (Bentley et al, 2015; Buelens et al, 2020; Cucchi et al, 2016; Schmaal & Bendall, 2018; Fox et al, 2015).
3. Target mechanisms with skills-based care. Treatments that strengthen emotion identification/tolerance, cognitive flexibility, and interpersonal effectiveness (e.g., DBT-informed skills) are well-matched to the functions and mechanisms outlined above; early work also supports brief transdiagnostic, emotion-focused approaches (Saccaro et al, 2024).

Psychological factors, although crucial, are only one of the contributing aspects. We look next at social factors which are relevant in cases of self-harm.

Social factors in NSSI

While NSSI is primarily conceptualised as an intrapersonal strategy for regulating affect, social environments play a profound role in its development, maintenance, and resolution. Social factors include family dynamics, peer relationships, cultural norms, stigma, and broader social contexts such as online communities. Understanding these influences is essential for accurate assessment and effective intervention.

Family and early environment

Parental relationships and attachment. Negative family environments—including low parental warmth, high criticism, inconsistent discipline, and invalidation of emotions—are strongly associated with NSSI onset. Adolescents with insecure attachment styles, particularly anxious or disorganised attachment, are at higher risk of using self-harm as a means of regulating interpersonal distress (Rogier et al, 2017). Invalidation, as conceptualised in Linehan’s biosocial theory, teaches youth to distrust their own emotional experiences, pushing them toward maladaptive coping such as NSSI (Adrian et al., 2011).

Childhood adversity. Social experiences of maltreatment, including physical, sexual, and emotional abuse or neglect, predict later engagement in NSSI. Meta-analyses confirm that all forms of childhood maltreatment significantly increase risk (Liu et al., 2018). Social isolation during childhood or adolescence also magnifies vulnerability, with lack of protective relationships exacerbating the need for intrapersonal coping strategies.

Peer influence and social contagion

Peer relationships. Adolescents who experience bullying, peer rejection, or social exclusion are at increased risk of NSSI (Martin et al, 2016; Heilbron & Prinstein, 2010). Victimisation heightens distress and reinforces negative self-concepts, while the absence of supportive peers reduces access to adaptive emotion regulation. Conversely, supportive friendships can serve as a protective factor.

Social contagion. Exposure to NSSI among peers can increase the likelihood of engagement. Adolescents in inpatient or residential settings often report that learning about peers’ NSSI normalised the behaviour, sometimes even providing methods (Jarvi et al., 2013). This contagion effect reflects both modelling and the perception that NSSI functions as an acceptable means of coping in certain peer contexts.

Cultural norms and stigma

Cultural attitudes toward mental health and emotional expression shape the visibility and acceptability of NSSI. In cultures where mental illness is stigmatised or emotional expression is discouraged, individuals may resort to self-harm in secrecy. Research across countries suggests that NSSI prevalence and correlates vary, but underlying social mechanisms—such as stigma, shame, and suppression of distress—are consistent (Muehlenkamp et al., 2012).

Online communities

The digital environment has emerged as a significant social context for NSSI. Online forums and social media may provide support, validation, and a sense of community for those who self-injure. However, they may also normalise or reinforce NSSI by sharing methods or glamorising the behaviour. Studies indicate that exposure to online NSSI content can increase risk for vulnerable individuals (Lewis & Seko, 2016).

With so many social factors impacting self-harm, mental health professionals may wonder how they can counter the influences. Gaining clarity on the clinical implications of social-factor influence is a valid first step.

Clinical implications

Assessment of social context. Clinicians must evaluate not only the intrapersonal functions of NSSI but also the social environment. This includes assessing family communication patterns, peer influences, experiences of bullying, and exposure to NSSI in peer groups or online. Family and social histories should be integrated into risk assessments.

Family interventions. Family-based approaches are critical, particularly in adolescents. Interventions such as attachment-based family therapy (Diamond et al., 2019) aim to improve communication, validate emotional experiences, and rebuild supportive bonds. Psychoeducation for families helps reduce invalidation and misunderstanding of NSSI.

Peer and school-based prevention. Because peer contagion plays a role, group interventions must be carefully structured to avoid inadvertently reinforcing NSSI. School-based programs should emphasise resilience, emotional literacy, and anti-bullying strategies, while ensuring safe discussion spaces without overexposure to triggering details (Jarvi et al, 2013; Heilbron & Prinstein, 2010).

Cultural competence. Clinicians should attend to cultural beliefs about mental health, stigma, and emotional expression. Interventions that normalise help-seeking, validate cultural identity, and adapt to cultural values improve engagement and outcomes (Muehlenkamp et al, 2012).

Digital context monitoring. Clinicians should inquire about online activity, as digital spaces can influence self-harm behaviours. Encouraging safer online practices, directing individuals to moderated support communities, and discussing potential risks of unregulated forums are increasingly important clinical tasks (Lewis & Seko, 2016).

Therapeutic alliance. Stigma around NSSI often leads to secrecy and shame. Clinicians must foster a nonjudgmental, validating therapeutic environment. Exploring the interpersonal functions of NSSI openly can strengthen alliance and reduce resistance (Craigen & Foster, 2009).

The big picture on social factors

Social factors—including family invalidation, peer rejection, contagion effects, cultural norms, and online communities—interact with intrapersonal vulnerabilities to shape the onset and maintenance of NSSI. Clinically, these insights highlight the need for systemic, context-sensitive approaches. Interventions must extend beyond individual emotion regulation skills to include family-based therapy, school prevention, culturally competent care, and digital literacy. By addressing both intrapersonal and social dynamics, clinicians can more effectively reduce NSSI and support healthier pathways for emotional expression (Diamond et al, 2019; Adrian et al, 2011; Lewis & Seko, 2016; Muehlenkamp et al, 2012; Jarvi et al, 2013; Heilbron & Prinstein, 2010).

Neuroscientific and biological factors

Finally, recent discoveries in neuroscience have demonstrated that, in addition to psychological and social factors, certain neurobiological markers tend to differentiate those who self-harm from those who do not.

Pain processing and analgesia

People who repeatedly engage in NSSI often show a higher tolerance for pain, reporting less discomfort during lab-based pain tasks. This has been observed in both adolescents and adults. Brain imaging and physiological studies suggest that their natural pain-blocking systems may work differently, and that the way their brains process pain signals and regulate them is altered. Functional MRI also shows differences in how the brain’s reward and pain-relief systems respond during self-inflicted pain—for example, changes in communication between regions like the orbitofrontal cortex and cingulate, as well as relief-related signals in the striatum and thalamus.

Taken together, these findings point to a “pain-insensitive” profile that may be present in some individuals who self-injure. Importantly, such alterations are not limited to pain processing alone. Adolescents with NSSI also show differences in how their stress systems respond (Osuch et al, 2014).

Stress-response systems (HPA axis and autonomic function)

Adolescents who engage in NSSI often show a reduced cortisol response to social stress tests (such as the Trier Social Stress Test), even though they report feeling highly distressed. This suggests that the hypothalamic–pituitary–adrenal (HPA) stress system may not be functioning normally. Studies looking at stress and pain together also find unusual patterns in cortisol levels, heart rate variability, and sympathetic nervous system activity, pointing to disrupted connections between stress and pain responses. While not all findings are consistent—some studies do report higher cortisol during pain—the overall evidence supports the idea that stress-system dysregulation is linked to NSSI, especially in its role as a way to reduce tension (Plener et al, 2017; Kaess et al, 2012; Koenig et al, 2009).

Cortico-limbic circuits for emotion, salience, and social threat

Neuroimaging studies in young people link NSSI to altered brain activity and connectivity across several key regions, including the amygdala, hippocampus, anterior cingulate cortex (ACC), insula, and prefrontal control areas. Both pilot and larger studies show that these youth often display heightened reactivity in limbic and ACC regions when processing emotional cues, unusual insula responses to painful or unpleasant sensory input, and distinct network patterns during experiences of social exclusion. Together, these findings suggest a pattern of increased sensitivity to emotionally and socially salient information, paired with reduced effectiveness of top-down regulatory control (Brown et al, 2017; Branas et al, 2021; Plener et al, 2012).

Candidate neuromodulators

One long-standing theory is that self-injury may temporarily increase the release of the body’s natural opioids, creating short-term relief and reinforcing the self-harm behaviour. Some reviews highlight early clinical evidence that opioid-blocking medications (such as naltrexone) might reduce self-injurious behaviours more broadly. However, when it comes to NSSI specifically, the findings are limited and inconsistent, and no medication has yet been proven effective as a treatment for NSSI itself (Karakula et al, 2024; Kirtley et al, 2015).

Overall, converging evidence suggests that NSSI is linked to distinctive alterations across all these systems, which together may help explain both the immediate relief and the reinforcing cycle of the behavior. Thus, we must ask: what do we need to do as clinicians now that we know this? We look at the clinical implications.

Clinical implications

1. Do not rely on pain as a deterrent. So, let’s say you have a self-injuring female client. Do you tell her not to keep cutting and banging because “it will hurt”? No. As we have just noted with the research findings above, people who engage NSSI typically have demonstrable hypoalgesia and robust pain-inhibitory engagement (that is, pain hurts them less than it does others and they have well-established means of inhibiting pain), so telling them it will hurt is not a persuasive prevention message. Instead, assess pain perception explicitly, monitor for severe tissue damage, and teach rapid, safer sensory strategies (e.g., suggest strategies such as cold-water holds or paced breathing) that can mimic relief without injury (Lalouni et al, 2022).
2. Target stress-system dysregulation. Incorporate interventions that down-shift physiological arousal and recalibrate HPA/ANS responses. Here we mean skills from Dialectical Behavioural Therapy (DBT) or unified protocols focusing on distress tolerance, emotion labelling, or diaphragmatic breathing. Basically, you are trying to bring the person back into their window of tolerance (see Mental Health Academy courses such as Widen the Window of Tolerance: Three Proven Ways to Support Clients’ Resilience, by Dr. David Treleaven).You can also use adjunctive therapies like biofeedback and sleep and activity regularisation, and track cortisol-linked symptoms (e.g., diurnal fatigue, stress reactivity) when feasible in research-informed settings (Koenig et al, 2017; Kaess et al, 2012).
3. Strengthen cortico-limbic regulation. Choose treatments that enhance prefrontal control over limbic/salience circuits. That is, you are looking to help the client exert more rational, executive (pre-frontal cortex) control over their emotional limbic system. Thus, interventions improving emotion-regulation and interpersonal-effectiveness skills plus mindfulness practices with interoceptive grounding will be most useful. Early evidence suggests neural connectivity changes may accompany symptom improvement; this sort of experimental neuromodulation is under investigation (Plener et al, 2017).

The neurobiology big picture

Summarising the neuroscientific and biological research findings, we can see that NSSI is associated with distinctive changes across pain, stress, emotional, and opioid-related systems. These alterations appear to work in combination; heightened tolerance for pain, blunted or atypical stress responses, increased sensitivity to emotionally salient cues, and potential short-term opioid release may all contribute to why self-injury provides immediate relief and becomes self-reinforcing. At the same time, compromised top-down regulatory control may make it harder for individuals to manage distress in healthier ways. Clinically, these findings underscore the importance of interventions that strengthen emotion regulation, stress tolerance, and alternative coping strategies, while highlighting why pharmacological treatments alone have not shown consistent benefit for NSSI.

Conclusion

Psychological, social, and neurobiological factors can all contribute to the development and maintenance of NSSI in a client. Different clinical implications are associated with each domain of factors, so it is crucial for clinicians to tease out which factors are relevant to a given client, enabling them to create individually tailored treatment plans. Only in this way can clinicians effectively reduce NSSI and support healthier pathways for emotional expression, thus helping those clients learn to meet more adaptively the needs they were attempting to meet through NSSI.

Key takeaways

• Psychological factors which generate and maintain NSSI include emotional dysregulation, cognitive-affective vulnerabilities, and interpersonal and developmental contexts which escalate suicidality; numerous disorders are comorbid with psychological factors.
• Social factors related to NSSI are those of family and early environment problems, social contagion (e.g., peer influence), cultural norms and stigma, and negatively-influencing online communities.
• Neurobiological factors associated with NSSI revolve around brain and body systems which function differently than in people who do not self-harm. These include pain processing sensitivities, the HPA and other stress-response systems, the cortico-limbic circuits, and candidate neuromodulators.
• The wide-ranging clinical implications for the aetiological factors point to thorough, comprehensive assessment (including for comorbidity), teaching DBT- and trauma-informed skills, family involvement, culturally competent interventions, and re-regulating imbalanced brain systems.

Questions therapists often ask

Q: How do I differentiate NSSI from a suicide attempt when clients minimise the behaviour?

A: Focus on intent, function, and expectation of outcome. The article emphasises that NSSI is typically used to regulate overwhelming affect, not to end life. Explore what the client hoped would happen during and after the act. Many clients use NSSI to stay alive by reducing distress, which helps clarify risk without relying on their reassurance alone.

Q: What early developmental factors should I pay closest attention to when formulating?

A: Disrupted attachment, inconsistent caregiving, and early environments that invalidated emotional states are key contributors. These experiences set the groundwork for poor emotion regulation and self-soothing deficits, which often show up later as NSSI. When assessing, look for patterns of emotional dismissal or chaotic care that shaped the client’s regulation strategies.

Q: How should I approach clients who insist their NSSI is “not a big deal”?

A: The article makes it clear that minimisation is common. Don’t challenge it head-on; instead, validate the function the behaviour serves and explore its role in the client’s emotional economy. When clients feel understood rather than pathologised, they’re more willing to examine risks, triggers, and alternative coping methods.

Q: What is most important to assess when identifying the function of NSSI?

A: Clarify the emotional sequence: what internal or interpersonal state precedes the behaviour, what relief or outcome follows, and how the behaviour fits the client’s coping repertoire. The article highlights functions such as affect regulation, communication, or self-punishment. Mapping these helps you target interventions that genuinely replace the behaviour rather than simply instructing the client to “stop.”

Q: How can I work with the interplay between trauma and NSSI without overwhelming the client?

A: Stay grounded in stabilisation. The article notes that trauma histories often underpin emotion dysregulation, but diving straight into trauma processing can escalate risk. Prioritise skills that enhance safety, distress tolerance, and emotional literacy. As the client builds capacity, you can gradually link past experiences to current impulses without reactivating trauma in a way that drives further NSSI.

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