Component

Paraxanthine

Paraxanthine. 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 acts on it

  1. Caffeine N3-demethylation produced the specified dimethylxanthine; fluvoxamine reduced its formation clearance.

    Caffeine → Paraxanthine source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers.
    limitations
    CYP1A2 is the principal demethylating route; minor routes and individual clearance vary.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    Caffeine produces a distinct metabolite that needs its own record.
    primary_references
    A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 172–178

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. · source_derived_draft · unverified_draft

    ## caf-met-px Caffeine produces a distinct metabolite that needs its own record. Caffeine N3-demethylation produced the specified dimethylxanthine; fluvoxamine reduced its formation clearance. Model: Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. Limitations: CYP1A2 is the principal demethylating route; minor routes and individual clearance vary. Evidence access: Primary abstract A fluvoxamine-caffeine interaction study. · 1996 · https://pubmed.ncbi.nlm.nih.gov/8807660/ · DOI 10.1097/00008571-199606000-00003
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The paraxanthine-to-caffeine ratio was used to phenotype CYP1A2 during smoking cessation.

    Human cytochrome P450 1A2 → Caffeine source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dim-research/15289794.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2", "start_char": 0, "end_char": 1753, "text_sha256": "90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2"}
    experimental_model
    Repeated caffeine phenotyping after smoking cessation
    exposure
    Abrupt cessation after run-in; repeated 148-mg caffeine probe doses
    limitations
    Smoking-cessation kinetics cannot be assigned to starting or stopping DIM. Clinical dose management requires drug-specific monitoring.
    nutrient_topic
    Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
    organism
    12 heavy smokers
    plain_language
    Caffeine provides a measurable probe of enzyme activity.
    primary_references
    [dim-p15289794] Time response of cytochrome P450 1A2 activity on cessation of heavy smoking. (2004). https://pubmed.ncbi.nlm.nih.gov/15289794/ DOI: 10.1016/j.clpt.2004.04.003
    tissue_or_cell_type
    CYP1A2 activity and caffeine clearance

    Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 831–842

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Repeated caffeine phenotyping after smoking cessation · source_derived_draft · unverified_draft

    ### dim-caffeine-1a2 The paraxanthine-to-caffeine ratio was used to phenotype CYP1A2 during smoking cessation. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Caffeine provides a measurable probe of enzyme activity. organism: 12 heavy smokers tissue_or_cell_type: CYP1A2 activity and caffeine clearance experimental_model: Repeated caffeine phenotyping after smoking cessation limitations: Smoking-cessation kinetics cannot be assigned to starting or stopping DIM. Clinical dose management requires drug-specific monitoring. exposure: Abrupt cessation after run-in; repeated 148-mg caffeine probe doses evidence_span: {"source_cache": "artifacts/dim-research/15289794.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2", "start_char": 0, "end_char": 1753, "text_sha256": "90eb96e72afdbbb53c322c2be9a34e5aa523c27f2fd0995a8eb224e2ec6e35e2"} [dim-p15289794] Time response of cytochrome P450 1A2 activity on cessation of heavy smoking. (2004). https://pubmed.ncbi.nlm.nih.gov/15289794/ DOI: 10.1016/j.clpt.2004.04.003
    Complete structured claim and evidence

  2. In human liver microsomes, fluvoxamine inhibited caffeine demethylated-metabolite formation with Ki values of 0.08–0.28 micromolar.

    Fluvoxamine → Human cytochrome P450 1A2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human liver microsomes; metabolite HPLC.
    limitations
    Not all three demethylations are exclusively CYP1A2-dependent.
    nutrient_topic
    Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
    plain_language
    An enzyme experiment supports the observed clearance interaction.
    primary_references
    Fluvoxamine is a potent inhibitor of the metabolism of caffeine in vitro. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9868741/ · DOI 10.1111/j.1600-0773.1998.tb01476.x

    Caffeine: receptors, metabolism, nutrient interactions, adaptation and discovery questions (2026-09-18) · lines 212–218

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human liver microsomes; metabolite HPLC. · source_derived_draft · unverified_draft

    ## caf-cyp1a2-inhibition An enzyme experiment supports the observed clearance interaction. In human liver microsomes, fluvoxamine inhibited caffeine demethylated-metabolite formation with Ki values of 0.08–0.28 micromolar. Model: Human liver microsomes; metabolite HPLC. Limitations: Not all three demethylations are exclusively CYP1A2-dependent. Evidence access: Primary abstract Fluvoxamine is a potent inhibitor of the metabolism of caffeine in vitro. · 1998 · https://pubmed.ncbi.nlm.nih.gov/9868741/ · DOI 10.1111/j.1600-0773.1998.tb01476.x
    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.

    Evidence, AI assistance and curation standards