A key problem in studying a hypothesized spectrum of severity of delusional ideation is determining that ideas are unfounded. The first objective was to use virtual reality to validate groups of individuals with low, moderate, and high levels of unfounded persecutory ideation. The second objective was to investigate, drawing upon a cognitive model of persecutory delusions, whether clinical and nonclinical paranoia are associated with similar causal factors. Three groups (low paranoia, high nonclinical paranoia, persecutory delusions) of 30 participants were recruited. Levels of paranoia were tested using virtual reality. The groups were compared on assessments of anxiety, worry, interpersonal sensitivity, depression, anomalous perceptual experiences, reasoning, and history of traumatic events. Virtual reality was found to cause no side effects. Persecutory ideation in virtual reality significantly differed across the groups. For the clear majority of the theoretical factors there were dose–response relationships with levels of paranoia. This is consistent with the idea of a spectrum of paranoia in the general population. Persecutory ideation is clearly present outside of clinical groups and there is consistency across the paranoia spectrum in associations with important theoretical variables.

Insomnia is a potential cause of anxiety, depression, and anomalies of experience; separate research has shown that anxiety, depression and anomalies of experience are predictors of paranoia. Thus insomnia may contribute to the formation and maintenance of persecutory ideation. The aim was to examine for the first time the association of insomnia symptoms and paranoia in the general population and the extent of insomnia in individuals with persecutory delusions attending psychiatric services. Assessments of insomnia, persecutory ideation, anxiety, and depression were completed by 300 individuals from the general population and 30 individuals with persecutory delusions and a diagnosis of non-affective psychosis. Insomnia symptoms were clearly associated with higher levels of persecutory ideation. Consistent with the theoretical understanding of paranoia, the association was partly explained by the presence of anxiety and depression. Moderate or severe insomnia was present in more than 50% of the delusions group. The study provides the first direct evidence that insomnia is common in individuals with high levels of paranoia. It is plausible that sleep difficulties contribute to the development of persecutory ideation. The intriguing implication is that insomnia interventions for this group could have the added benefit of lessening paranoia.

Depression is common in people with schizophrenia, but how it might directly contribute to the persistence of psychotic symptoms has rarely been tested. The key aim of the present study was to test whether depression and associated cognitive processes predict the maintenance of persecutory delusions. Three groups of participants were tested at baseline: 60 patients with persecutory delusions in the context of a schizophrenia spectrum diagnosis, 30 patients with depression, and 30 nonclinical controls. They completed interviewer and self-report assessments of depression and paranoia, and measures of six cognitive factors (schematic beliefs, experiential avoidance, autobiographical memory, problem solving, rumination, worry style). The patients with persecutory delusions were then assessed again, six months later. It was found that 50% of the patients with persecutory delusions met diagnostic criteria for major depression. Cognitive processes found to be associated with depression across the groups were negative schematic beliefs about the self, experiential avoidance and rumination, but not autobiographical memory or problem solving. The severity of initial depression in patients with persecutory delusions predicted the persistence of paranoia over six months. A number of cognitive factors also predicted the persistence of persecutory delusions, including negative schematic beliefs about the self, worry, and problem-solving difficulties. In conclusion, depression is common in patients with current persecutory delusions, and it shows similar cognitive features to major depressive disorder. The results of this study indicate that depression and related processes may contribute to the maintenance of paranoia. Trials are warranted of depression-related therapeutic techniques for people with persecutory delusions.

BackgroundBeing physically assaulted is known to increase the risk of the occurrence of post-traumatic stress disorder (PTSD) symptoms but it may also skew judgements about the intentions of other people. The objectives of the study were to assess paranoia and PTSD after an assault and to test whether theory-derived cognitive factors predicted the persistence of these problems.MethodAt 4 weeks after hospital attendance due to an assault, 106 people were assessed on multiple symptom measures (including virtual reality) and cognitive factors from models of paranoia and PTSD. The symptom measures were repeated 3 and 6 months later.ResultsFactor analysis indicated that paranoia and PTSD were distinct experiences, though positively correlated. At 4 weeks, 33% of participants met diagnostic criteria for PTSD, falling to 16% at follow-up. Of the group at the first assessment, 80% reported that since the assault they were excessively fearful of other people, which over time fell to 66%. Almost all the cognitive factors (including information-processing style during the trauma, mental defeat, qualities of unwanted memories, self-blame, negative thoughts about self, worry, safety behaviours, anomalous internal experiences and cognitive inflexibility) predicted later paranoia and PTSD, but there was little evidence of differential prediction.ConclusionsParanoia after an assault may be common and distinguishable from PTSD but predicted by a strikingly similar range of factors.

Various psychological and biological pathways have been proposed as mediators between childhood adversity (CA) and psychosis. A systematic review of the evidence in this domain is needed. Our aim is to systematically review the evidence on psychological and biological mediators between CA and psychosis across the psychosis spectrum. This review followed PRISMA guidelines. Articles published between 1979 and July 2019 were identified through a literature search in OVID (PsychINFO, Medline and Embase) and Cochrane Libraries. The evidence by each analysis and each study is presented by group of mediator categories found. The percentage of total effect mediated was calculated. Forty-eight studies were included, 21 in clinical samples and 27 in the general population (GP) with a total of 82 352 subjects from GP and 3189 from clinical studies. The quality of studies was judged as ‘fair’. Our results showed (i) solid evidence of mediation between CA and psychosis by negative cognitive schemas about the self, the world and others (NS); by dissociation and other post-traumatic stress disorder symptoms; and through an affective pathway in GP but not in subjects with disorder; (iii) lack of studies exploring biological mediators. We found evidence suggesting that various overlapping and not competing pathways involving post-traumatic and mood symptoms, as well as negative cognitions contribute partially to the link between CA and psychosis. Experiences of CA, along with relevant mediators should be routinely assessed in patients with psychosis. Evidence testing efficacy of interventions targeting such mediators through cognitive behavioural approaches and/or pharmacological means is needed in future.