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Cognitive impairments are a core feature of first-episode psychosis (FEP), arising before illness onset and antipsychotic exposure. Individuals with chronic psychosis experience poorer physical health while taking antipsychotic medication, but health disparities may be evident at FEP onset, prior to antipsychotic exposure. Given the links between cognition and physical health in healthy populations, the aim was to explore whether cognition and physical health are associated in FEP, which could inform early physical health interventions for cognition in FEP. Participants were aged 15 to 25 and included 86 individuals experiencing FEP with limited antipsychotic exposure and duration of untreated psychosis of ≤six months, and 43 age- and sex-matched controls. Individuals with FEP performed significantly poorer than controls in most cognitive domains (Cohen's d = 0.38 to 1.59). Groups were similar in metabolic health measures, excluding a significantly faster heart rate in FEP (d = 0.68). Through hierarchical regression analyses, we found that in the overall sample, BMI was negatively related to current IQ after controlling for education and group (FEP/control). Relationships between BMI and cognition were consistent across the FEP and healthy control groups. In FEP, current IQ and working memory were negatively correlated with lipid profiles. Findings suggest that in FEP, impaired cognition is exhibited earlier than physical health problems, and that compared to controls, similar relationships with cognition are demonstrated. Causal pathways and trajectories of relationships between health and cognition in FEP require investigation, especially as antipsychotic medications are introduced. The findings have implications for cognitive and health interventions.

Our understanding of the nature and aetiological architecture of psychotic mental disorders has advanced notably in the past 20 years. It is now widely considered that psychotic disorders occur as consequence of a complex range of factors, spanning multiple domains and levels, that act on several psychological and biological mechanisms. In recent years, evidence has accumulated that exposure to, broadly, adverse social conditions and experiences over the course of development constitute part of this complex array of factors that influence onset. In this chapter, we will provide a critical overview of this evidence, including consideration of outstanding conceptual and methodological issues that limit the causal inferences that can be drawn from existing findings. From this, we will propose and sketch a sociodevelopmental pathway—as one of several pathways—to psychoses.

Young people who have been identified as being at “ultra-high risk” (UHR) for psychosis are at even greater risk of developing a psychotic disorder if at the time of presentation, they also have a cannabis use disorder. Additionally, UHR individuals who experience attenuated psychotic symptoms induced by cannabis are nearly five times more likely to transition to a psychotic disorder than UHR individuals who do not experience cannabis-induced symptoms. There is also evidence that cannabis use could affect the early trajectory of psychotic disorders, as there is a higher proportion of cannabis users in UHR cohorts compared with healthy controls, and an earlier age at first cannabis use increases the risk of transition to psychosis. The majority of research to date on the connection between cannabis use and UHR has been descriptive or observational, but a number of potential therapeutic interventions for cannabis use in those at UHR have emerged, including psychosocial interventions like motivational interviewing. The therapeutic use of cannabidiol, which could reduce the risk of transitioning to a psychotic disorder in the UHR population, should also be studied.