Component
Pre-existing predisposition for psychosis
Pre-existing predisposition for psychosis. Species, exposure and limitations are retained in each linked claim.
1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
How nutrients influence it
Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
How nutrients reach it in more than one step
Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.
Tracing routes…
What it does
Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.
What it acts on
After adjustment for age, sex, socioeconomic status, urbanicity, childhood trauma, baseline predisposition and other drug, tobacco and alcohol use, cannabis use raised the cumulative incidence of psychotic symptoms four years later with an adjusted odds ratio of 1.67, and the effect was much stronger in those with any predisposition at baseline, a 23.8 percentage point risk difference against 5.6 in those without.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/thc-research/15574485.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56846f52ea834853e8aa27f64700905e072d53611066a7c58df74269b65ec290", "start_char": 0, "end_char": 1860, "text_sha256": "56846f52ea834853e8aa27f64700905e072d53611066a7c58df74269b65ec290"}
- experimental_model
- Prospective cohort of 2437 young people with baseline predisposition assessment
- exposure
- Cannabis use at baseline with psychotic symptoms at four-year follow-up
- limitations
- A prospective design with adjustment for predisposition, trauma and other drugs, which is what makes the interaction finding interpretable.
- nutrient_topic
- THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. · Delta-9-tetrahydrocannabinol / THC
- organism
- Human
- plain_language
- The risk lands overwhelmingly on people already predisposed.
- primary_references
- [thc-p15574485] Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. (2005). https://pubmed.ncbi.nlm.nih.gov/15574485/ DOI: 10.1136/bmj.38267.664086.63
- tissue_or_cell_type
- Whole body
THC: the cannabinoid receptors, the endocannabinoid system it occupies, what the drug does, and the dietary fat it is built from (2026-09-21) · lines 595–606
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective cohort of 2437 young people with baseline predisposition assessment · source_derived_draft · unverified_draft
### thc-psychosis-predisposition-interaction After adjustment for age, sex, socioeconomic status, urbanicity, childhood trauma, baseline predisposition and other drug, tobacco and alcohol use, cannabis use raised the cumulative incidence of psychotic symptoms four years later with an adjusted odds ratio of 1.67, and the effect was much stronger in those with any predisposition at baseline, a 23.8 percentage point risk difference against 5.6 in those without. Condition category: normal nutrient_topic: THC research collection; topical membership is not evidence of a direct clinical effect, and THC is recorded separately from the endocannabinoids it imitates. plain_language: The risk lands overwhelmingly on people already predisposed. organism: Human tissue_or_cell_type: Whole body experimental_model: Prospective cohort of 2437 young people with baseline predisposition assessment limitations: A prospective design with adjustment for predisposition, trauma and other drugs, which is what makes the interaction finding interpretable. exposure: Cannabis use at baseline with psychotic symptoms at four-year follow-up evidence_span: {"source_cache": "artifacts/thc-research/15574485.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "56846f52ea834853e8aa27f64700905e072d53611066a7c58df74269b65ec290", "start_char": 0, "end_char": 1860, "text_sha256": "56846f52ea834853e8aa27f64700905e072d53611066a7c58df74269b65ec290"} [thc-p15574485] Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. (2005). https://pubmed.ncbi.nlm.nih.gov/15574485/ DOI: 10.1136/bmj.38267.664086.63
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.