What is CHR-P?
The clinical high risk for psychosis (CHR-P) paradigm identifies individuals who show early, subthreshold signs of psychosis before a full psychotic disorder develops, with the goal of enabling early intervention to prevent or delay transition to psychosis.
History in a nutshell
The CHR-P paradigm emerged in the early 1990s through parallel developments across several research groups. Alison Yung and Patrick McGorry in Melbourne established the first dedicated at-risk clinic (PACE, 1994) and formalized the Ultra High Risk (UHR) criteria based on attenuated psychotic symptoms and functional decline. Around the same time, Thomas McGlashan and Scott Woods at Yale developed overlapping criteria and structured assessment tools, which became widely adopted in North American research. Concurrently, the basic symptoms approach was further developed by Joachim Klosterkötter, Anita Riecher-Rössler and colleagues in the German-speaking world, focusing on subtle, self-experienced neuropsychological disturbances as early indicators of psychotic vulnerability. These traditions have since been (sort-of) integrated and exported worldwide into the modern CHR-P framework. For a fairly recent overview see this study by Raballo et al. (2024).
Pros and cons
The CHR-P paradigm has been transformative in shifting psychiatry toward earlier identification and intervention, instead of a more reactive approach to established psychotic conditions. It has generated a substantial evidence base and led to the development of dedicated early intervention services that have helped many young people receive support before full psychotic breakdown. At the same time, the paradigm is not without flaws: the majority of those labeled CHR-P never develop psychosis, raising serious concerns about stigma, unnecessary anxiety, and potential overmedicalization of what may be transient distress. Critics have argued that the binary focus on "conversion" as the primary outcome reflects a narrow, disease-centered view that neglects broader functional and personal recovery outcomes, and that categorical risk labeling sits uneasily with the dimensional, continuous nature of psychotic experiences in the general population.
Personal contributions
My personal research contributions stem from my PhD project in Utrecht (2005-2010), which was focused on young CHR-P adolescents (12-18y). Interesting findings were, for example, evidence for early changes in cortical thickness and sensorimotor gating in those at risk, particularly for those later developing psychosis. On the other hand, the conversion rate in young adolescents appeared to be even lower than at a later age, further scrutinising the potential benefits of the paradigm in younger populations. Later on, our work was included in some large-scale collaborations to meta-analyse conversion rates and to optimize prediction models, e.g. most recently by Bonnet et al. (2025) The final prediction model in that study included disorders of thought content, disorganised speech and general functioning, which had fairly good predictive ability. Furthermore, two recent studies in the NICOTINE project showed that smoking was NOT related to structural (grey matter) or functional (resting-state) brain alterations in CHR-P youth.
Although I am currently not involved in new research projects including CHR-P individuals, my aim is to continue to contribute to the finetuning of screenings for psychosis-risk in the future, in particular for autism.