This paper examines the evidence that delusions can be explained within the framework of a neurocognitive model of how the brain assesses certainty. Here, 'certainty' refers to both low-level interpretations of one's environment and high-level (conscious) appraisals of one's beliefs and experiences. A model is proposed explaining how the brain systems responsible for assigning certainty might dysfunction, contributing to the cause and maintenance of delusional beliefs. It is suggested that delusions arise through a combination of perturbed striatal dopamine and aberrant salience as well as cognitive biases such as the tendency to jump to conclusions (JTC) and hypersalience of evidence-hypothesis matches. The role of emotion, stress, trauma and sociocultural factors in forming and modifying delusions is also considered. Understanding the mechanisms involved in forming and maintaining delusions has important clinical implications, as interventions that improve cognitive flexibility (e.g. cognitive remediation therapy and mindfulness training) could potentially attenuate neurocognitive processes.

Average well-being in people with psychosis was lower than SWB previously reported for the general population. Unemployment, lack of social support, poorer coping, and distressing beliefs were all associated with lower levels of well-being in people with psychosis. Psychological interventions targeting the positive symptoms of psychosis may impact on well-being. Greater focus on promoting social contact and inclusion and facilitating a return to employment may further improve well-being outcomes following psychological intervention. The cross-sectional design of the study does not allow for firm conclusions about the causal relationship between well-being and associated factors in psychosis. The study was carried out within a particular service context, and the findings need replicating before they can be considered to be generalizable outside this setting.

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Schizotypy refers to the continuum of normal variability of psychosis-like characteristics and experiences, often classified as positive schizotypy (‘unusual experiences’; UE) and negative schizotypy (‘introvertive anhedonia’; IA). Here, we investigated the link between schizotypy and cognitive processing style and performance. A particular focus was on whether schizotypy is associated more with Type 1 (automatic/heuristic) than Type 2 (reflective/effortful) processes, as may be expected from findings of impaired top-down control in schizophrenia. A large sample (n = 1,512) completed online measures pertaining to schizotypy (Oxford-Liverpool Inventory for Feelings and Experiences; O-LIFE), thinking style (Rational Experiential Inventory-10, Actively Open-Minded Thinking Scale), and reasoning performance (Cognitive Reflection Test). Higher positive (UE) and negative (IA) schizotypy were associated with more pronounced Type 1 processing, i.e. greater self-reported Faith in Intuition (FI), lower Need for Cognition (NFC), lower Actively Open-Minded Thinking (AOT), and lower cognitive reflection test (CRT) scores. Canonical correlation analysis confirmed a significant association between UE and increased FI, lower AOT and lower CRT performance, accounting for 12.38% of the shared variance between schizotypy and thinking dispositions. IA was more highly associated with reduced NFC. These findings suggest that schizotypy may be associated with similar thinking dispositions to those reported in psychosis, with different patterns of associations for positive and negative schizotypy. This result informs research on reasoning processes in psychosis and has clinical implications, including potential treatment targets and refinements for cognitive therapies.

Acute tryptophan depletion caused a significant decrease in perceived control and increase in interfering thoughts at the time of provocation. Acute tryptophan depletion had no effect on the Spielberger State Anxiety Inventory or Visual Analogue Scale Anxiety measures, which suggests that the mechanism of action of selective serotonin reuptake inhibitors may be different to that seen in panic, social anxiety and post-traumatic stress disorder. Successful selective serotonin reuptake inhibitor treatment of obsessive-compulsive disorder may involve the ability of serotonin to switch habitual responding to goal-directed behaviour.