Maltreatment by peers – or bullying – refers to the intentional, repeated and hurtful behaviour occurring between individuals of similar ages who do not possess equal power (Olweus, 1996). Psychosis is a symptom of severe mental disorders and is characterized by an impaired relationship with reality – examples of symptoms including hallucinations and delusions. Various mechanisms have been proposed to explain the link between these variables including biological and cognitive explanations as well as indirect mechanisms.
Regarding biological mechanisms, research has suggested that bullying may alter the physiological response to stress through the hypothalamic–pituitary–adrenocortical (HPA) axis (Ouellet-Morin et al. 2011). HPA alterations from early-life stress is found to significantly affect mental health, where increased sensitivity to stress can play a key role in psychotic disorders like schizophrenia (Schreier et al., 2009). Maladaptive HPA responses are characterized by reduced secretion of cortisol and claimed to heighten vulnerability to stress-related disorders (Ouellet-Morin et al. 2011) as well as psychotic symptoms (Kapur, 2003). Bullied children exhibited significantly lower cortisol responses to stress than non-bullied children (Ouellet-Morin et al. 2011). The role of peer maltreatment on HPA alterations is further supported by the dose-response relationship found between more frequent, severe and chronic experiences and lower cortisol secretion. Moreover, in response to possible environmental threats, bullies are found to not only show increased reactivity (Sterzer & Stadler, 2009) but also maladaptive HPA responses (van Bokhoven et al. 2005) – the combination putting them at elevated psychotic risk (Bradley & Dinan, 2010). At an even larger risk for depression and psychosis are bully/victims, argued to have the most cognitive and biological alterations, due to possessing qualities of both bullies and victims. Adverse experiences typically make individuals vulnerable to psychotic symptoms by increasing their emotional reactivity to future stressors (Mackie et al. 2011).
Other biological mechanisms are telomere length (Shalev et al. 2013) and the epigenome (Ouellet-Morin et al. 2013). Telomere length was linked to risk factors that predict psychotic disorders. For example, patients with schizophrenia had a shorter mean telomere length than controls (Yu et al. 2008). One suggested cause for telomere erosion is frequent childhood victimisation (Shalev et al. 2013). As mentioned, decreased cortisol reactions to stress is suggested to affect mental health. Another factor found to reduce cortisol is increased levels of SERT methylation (Ouellet-Morin et al. 2011). These increased levels were found to be exhibited more in bullied twins than their non-bullied monozygotic twin.
Bullying may also lead to cognitive alterations where bullied children may develop negative schemas about the self and the world (Gracie et al. 2007) and become overly sensitive to negative environmental cues (Crittendon & Ainsworth, 1989). They may, for example, get suspicious of intentions, predisposing themselves to psychotic symptoms like paranoia (Morrison et al, 2003). The presence of negative schemas thus produces a cognitive vulnerability to psychotic-like experiences (Birchwood et al. 2004). Similarly, bullying can increase the levels of self-blaming cognitions (Perren, Ettekal & Ladd, 2013) – distortions in interpreting the environment such as wrongly attributing sources of negative events to themselves (Kinderman & Bentall, 1996). The association between non-clinical psychotic symptoms and victimization is only present for self-reported maltreatment and not in peer-reported bullying, possibly highlighting this interpretation bias (Gromann et al., 2013). Children with elevated levels of self-blaming attributions and who suffered from peer maltreatment are more likely to develop internalizing problems than those with lower self-blaming attributions (Perren, Ettekal & Ladd, 2013). Furthermore, social adversity is also linked to negative emotion processing. Identifying social cues is an important skill in developing successful relationships (Pollak & Sinha, 2002). However, the risk of psychopathology increases when one is overly sensitive to such cues (Arseneault, Bowes, & Shakoor, 2010). Bullied children may more rapidly and accurately detect expressions of anger – impacting their behavior and interactions. The effect of social adversity on increased psychotic risk can also be explained by the ‘social defeat hypothesis’ (Selten et al., 2013). This is the negative and long-term experience of being excluded from majority groups – found to elevate the risk of not only psychotic symptoms but also disorders like schizophrenia.
Lastly, depression has been found to be an indirect mechanism between peer victimization and presence of psychotic experiences (Fisher et al., 2013). Extensive research demonstrates the elevated risks of depression from bullying (Copeland et al. 2013) and that affective disorders like depression are additional risks for experiencing psychotic symptoms (Garety et al., 2007). Another indirect mechanism could be cannabis use. Regardless of the type of bullying (Tharp-Taylor, Haviland & D’Amico, 2009) and even after controlling for prior influences (Kim et al., 2011), research shows an association between bullying victimization and cannabis use (Martino, Collins, & Ellickson, 2004). Additionally, cannabis use and psychotic experiences are found to be significantly linked (Mackie et al., 2011).
This leads to the idea that bullying may also be a developmental marker and not a cause for an elevated risk of psychotic symptoms (Kelleher et al., 2013). This means that bullying may be a by-product of something else elevating the risk such as poor social adjustment (Done et al. 1994) due to factors like being bad at sports (Schreier et al., 2009). Although bullying may result from social issues, because of existing risks for psychosis, the additional effect of bullying could further increase psychotic risk.
In conclusion, it is concerning that any bullying role can elevate psychotic risk in adolescence (Wolke et al., 2014) because these symptoms are found to increase the likelihood of psychiatric disorders (Fisher et al. 2013) and suicide attempts (Kelleher et al., 2013). Enhanced understanding of the mechanisms is crucial to allow appropriate interventions to be implemented, possibly preventing the development of psychotic disorders. There remains a need for the exact mechanisms to be clarified. For example, although a reduction in cortisol has been linked to higher rates of disorder, a few studies have found both hyper-secretion and hypo-secretion of cortisol in bullied boys and girls respectively (Vaillancourt et al., 2008). Nevertheless, there are multiple psychotic symptoms and so finding and explaining all the possible mechanisms is difficult.