Causes and risk factors

Bullying victimisation increases the risk of emergence and persistence of specific psychotic symptoms and of psychotic disorder

ABSTRACT FROM: Catone G, Marwaha S, Kuipers E, et al. Bullying victimisation and risk of psychotic phenomena: analyses of British national survey data. Lancet Psychiatry 2015;2:618–24.

What is already known on this topic

There is a strong association between social influences and adversities, and the emergence of psychosis, with urban upbringing, migrant status, childhood abuse and neglect, parental death, family breakdown, school mobility, and social disadvantage and marginalisation, all increasing the risk of psychotic symptoms.1–3 One such influence is bullying victimisation. The relationship between being bullied and specific psychotic symptoms or a psychotic disorder has not been fully elucidated.

Methods of the study

Catone and colleagues analysed data from the 2000 and 2007 British Adult Psychiatric Morbidity Surveys, including 18-month follow-up data, for a subsample of respondents in the 2000 survey, making this both a cross-sectional and longitudinal study. Assessments were conducted over two phases—phase 1: an interview with questionnaires on experiences of adverse events and traumas including being bullied and phase 2: a Schedules for Clinical Assessment in Neuropsychiatry (SCAN) interview. Items from the Psychosis Screening Questionnaire were used to identify persecutory ideation and hallucinatory experiences. A diagnosis of ‘probable psychosis’ was made either on the SCAN interview or in those not interviewed, using predetermined criteria such as current antipsychotic medication use, a recent psychiatric hospital admission, self-reported diagnosis, or symptoms suggestive of a psychotic disorder. Logistic regression analyses were conducted to explore independent associations between bullying victimisation and specific psychotic symptoms or a diagnosis of probable psychosis, controlling for sociodemographics (including ethnicity), IQ and trauma-related variables.

What this paper adds

  • The 2000 and 2007 data sets had 8580 and 7403 respondents, respectively, making this a very large sample.

  • Separate analyses of the two data sets allowed an ‘internal replication’ of the results. Bullying victimisation independently increased the risk of persecutory ideation and hallucinatory experiences about twofold each, with a fourfold risk for both symptoms being present together.

  • Bullying victimisation was significantly associated with a diagnosis of probable psychosis (2000 survey: OR 3.91, 95% CI 2.16 to 7.07; 2007 survey: OR 3.43, 95% CI 1.67 to 7.03), but this did not reach levels of significance after adjusting for confounders.

  • Bullying victimisation was associated with a twofold increased risk of both incident persecutory ideation (reported for the first time at follow-up assessment) and persistence of these symptoms among those who had reported these at baseline assessment. The emergence of hallucinations seemed to be predicted by bullying in a similar way, but at lower levels of significance.

Limitations

  • Retrospective recall of subjective adversities such as bullying may be inaccurate and also prone to ‘effort after meaning’ bias.

  • National morbidity surveys are inherently different from individual mental state examinations. Data on individual psychopathology collected in such surveys is prone to inaccuracies. In this study, phase 2 of data collection used SCAN interviews, which are very detailed standardised interviews, and mental state examination. The phase 1 screening could have missed probable cases, however, a sample size of 1600 with a detailed screen based on face-to-face psychiatric assessment of sufficient research rigour may be unfeasible, and thus a pay off between detail and sample size is required.

  • Further carefully designed prospective studies are needed to determine the chronological relationship between exposure (being bullied) and outcome (psychotic symptoms) and/or to separate the effect of childhood versus lifetime bullying.

What next in research?

  • Using a prospective studies design, we need to understand the causal mechanisms, both biological and psychological, by which social adversities produce psychotic symptoms.

  • Intervention studies are needed to determine the added value of psychotherapeutic interventions that specifically target past adverse social experiences. We are beginning to understand how early life experiences and social adversity can sensitise the dopaminergic system in the brain, making it both more prone to stress and also distorting cognitive schema towards paranoia.1 Exploring the specific effect of psychotherapies on neurophysiological dysfunction and potential reversal of such brain change should soon be within our research capabilities.

Do these results change your practices and why?

Probably, yes. Treatment of psychotic disorders was revolutionised following the introduction of antipsychotics. Extensive and expensive research into genetics and neuroimaging has improved our understanding of the biochemical mechanism of the genesis of psychotic symptoms, without commensurate advances in biological treatments. Hopefully, this will change as we understand the dynamic brain processes that accompany emerging psychosis, and develop targeted biological treatments. Meanwhile, recent innovations in psychological treatments, such as changing a patient's beliefs about the power and omnipotence of hallucinatory voices,4 offer the possibility of new forms of psychological interventions. I have started exploring bullying experiences as a routine part of my clinical assessment of psychosis. Exploring past adverse events not only improves the quality of therapeutic engagement, by making patients feel understood, it also opens up avenues for specific psychotherapeutic interventions.

  • Competing interests: None declared.

  • Provenance and peer review: Commissioned; internally peer reviewed.

  1. close Howes OD, Murray RM. Schizophrenia: an integrated sociodevelopmental-cognitive model. Lancet 2014; 383:1677–87.
  2. close Van Winkel R, van Nierop M, Myin-Germeys I, et al. Childhood trauma as a cause of psychosis: linking genes, psychology and biology. Can J Psychiatry 2013; 58:44–51.
  3. close Singh SP, Winsper C, Wolke D, et al. School mobility and prospective pathways to psychotic-like symptoms in early adolescence: a prospective birth cohort study. J Am Acad Child Adolesc Psychiatry 2014; 53:587–27.
  4. close Birchwood M, Michail M, Meaden A, et al. Cognitive behavior therapy to prevent harmful compliance with command hallucinations (COMMAND); a randomised controlled trial. Lancet Psychiatry 2014; 1:23–33.

  • Received: 10 September 2015
  • Accepted: 1 December 2015
  • First published: 30 December 2015
  • Online issue publication: 21 January 2016

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