Component

Cannabis use

Cannabis use. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What it acts on

  1. Higher levels of cannabis use were associated with increased risk for psychosis in all included studies, with an odds ratio of 3.90 for schizophrenia and other psychosis-related outcomes among the heaviest users compared with non-users, across 66,816 individuals.

    Cannabis use → Psychotic symptoms source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/26884547.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f62f6a3846a5e753f3268581ec2d6cedb08c6844df6ba9dd32f74bc09947231", "start_char": 0, "end_char": 1584, "text_sha256": "4f62f6a3846a5e753f3268581ec2d6cedb08c6844df6ba9dd32f74bc09947231"}
    experimental_model
    Systematic review and meta-analysis of 10 studies and 66,816 individuals
    exposure
    Level of cannabis consumption before psychosis onset
    limitations
    A dose-response meta-analysis of observational studies. Observational designs cannot separate use that causes psychosis from use that precedes it for other reasons.
    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 heaviest users had about four times the risk, and the risk rose with the amount used.
    primary_references
    [thc-p26884547] Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis. (2016). https://pubmed.ncbi.nlm.nih.gov/26884547/ DOI: 10.1093/schbul/sbw003
    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 582–593

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Systematic review and meta-analysis of 10 studies and 66,816 individuals · source_derived_draft · unverified_draft

    ### thc-psychosis-dose-response Higher levels of cannabis use were associated with increased risk for psychosis in all included studies, with an odds ratio of 3.90 for schizophrenia and other psychosis-related outcomes among the heaviest users compared with non-users, across 66,816 individuals. 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 heaviest users had about four times the risk, and the risk rose with the amount used. organism: Human tissue_or_cell_type: Whole body experimental_model: Systematic review and meta-analysis of 10 studies and 66,816 individuals limitations: A dose-response meta-analysis of observational studies. Observational designs cannot separate use that causes psychosis from use that precedes it for other reasons. exposure: Level of cannabis consumption before psychosis onset evidence_span: {"source_cache": "artifacts/thc-research/26884547.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4f62f6a3846a5e753f3268581ec2d6cedb08c6844df6ba9dd32f74bc09947231", "start_char": 0, "end_char": 1584, "text_sha256": "4f62f6a3846a5e753f3268581ec2d6cedb08c6844df6ba9dd32f74bc09947231"} [thc-p26884547] Meta-analysis of the Association Between the Level of Cannabis Use and Risk of Psychosis. (2016). https://pubmed.ncbi.nlm.nih.gov/26884547/ DOI: 10.1093/schbul/sbw003
    Complete structured claim and evidence

  2. Cannabis use was associated with an earlier onset of psychosis in a systematic meta-analysis.

    Cannabis use → Age at onset of psychosis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/thc-research/21300939.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89d48d713734797db84d74790a6a0eb51c99f4a40f9d7e6b64fd57edf4c0c0f5", "start_char": 0, "end_char": 1963, "text_sha256": "89d48d713734797db84d74790a6a0eb51c99f4a40f9d7e6b64fd57edf4c0c0f5"}
    experimental_model
    Systematic meta-analysis of age at onset of psychosis in cannabis users
    exposure
    Cannabis use against age at psychosis onset
    limitations
    Measures timing rather than incidence. Earlier onset in users is consistent with precipitation, with confounding, or with both.
    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
    Among people who develop psychosis, users develop it younger.
    primary_references
    [thc-p21300939] Cannabis use and earlier onset of psychosis: a systematic meta-analysis. (2011). https://pubmed.ncbi.nlm.nih.gov/21300939/ DOI: 10.1001/archgenpsychiatry.2011.5
    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 608–619

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Systematic meta-analysis of age at onset of psychosis in cannabis users · source_derived_draft · unverified_draft

    ### thc-psychosis-earlier-onset Cannabis use was associated with an earlier onset of psychosis in a systematic meta-analysis. 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: Among people who develop psychosis, users develop it younger. organism: Human tissue_or_cell_type: Whole body experimental_model: Systematic meta-analysis of age at onset of psychosis in cannabis users limitations: Measures timing rather than incidence. Earlier onset in users is consistent with precipitation, with confounding, or with both. exposure: Cannabis use against age at psychosis onset evidence_span: {"source_cache": "artifacts/thc-research/21300939.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89d48d713734797db84d74790a6a0eb51c99f4a40f9d7e6b64fd57edf4c0c0f5", "start_char": 0, "end_char": 1963, "text_sha256": "89d48d713734797db84d74790a6a0eb51c99f4a40f9d7e6b64fd57edf4c0c0f5"} [thc-p21300939] Cannabis use and earlier onset of psychosis: a systematic meta-analysis. (2011). https://pubmed.ncbi.nlm.nih.gov/21300939/ DOI: 10.1001/archgenpsychiatry.2011.5
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. 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.

    Pre-existing predisposition for psychosis → Psychotic symptoms source_derived_draftungraded
    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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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