Component
Caffeine clearance
Caffeine clearance. Species, exposure and limitations are retained in each linked claim.
3 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 acts on it
Nicotine patches did not significantly change caffeine pharmacokinetics or metabolite formation in the crossover study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dim-research/21599724.publisher-preview.txt", "locator": "Primary public publisher preview, reference superscripts removed; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a31ba5c71ba785b8fc6cdec21ed2dfa37686cb6d44dbf22616b0ab9b585a940", "start_char": 0, "end_char": 537, "text_sha256": "2a31ba5c71ba785b8fc6cdec21ed2dfa37686cb6d44dbf22616b0ab9b585a940"}
- experimental_model
- Randomized crossover nicotine-patch study; full-text extract
- exposure
- 42 mg/day transdermal nicotine or placebo; caffeine probe on day eight
- limitations
- Nicotine-only exposure differs from smoke exposure; this short study does not test every tissue or nicotine product.
- nutrient_topic
- Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
- organism
- 12 healthy smokers abstinent from tobacco during study
- plain_language
- Smoking and nicotine alone are not interchangeable CYP1A2 exposures.
- primary_references
- [dim-p21599724] Effect of nicotine on cytochrome P450 1A2 activity. (2011). https://pubmed.ncbi.nlm.nih.gov/21599724/ DOI: 10.1111/j.1365-2125.2011.04023.x
- tissue_or_cell_type
- Caffeine-based hepatic CYP1A2 phenotyping
Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 857–868
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized crossover nicotine-patch study; full-text extract · source_derived_draft · unverified_draft
### dim-nicotine-not-smoke Nicotine patches did not significantly change caffeine pharmacokinetics or metabolite formation in the crossover study. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Smoking and nicotine alone are not interchangeable CYP1A2 exposures. organism: 12 healthy smokers abstinent from tobacco during study tissue_or_cell_type: Caffeine-based hepatic CYP1A2 phenotyping experimental_model: Randomized crossover nicotine-patch study; full-text extract limitations: Nicotine-only exposure differs from smoke exposure; this short study does not test every tissue or nicotine product. exposure: 42 mg/day transdermal nicotine or placebo; caffeine probe on day eight evidence_span: {"source_cache": "artifacts/dim-research/21599724.publisher-preview.txt", "locator": "Primary public publisher preview, reference superscripts removed; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2a31ba5c71ba785b8fc6cdec21ed2dfa37686cb6d44dbf22616b0ab9b585a940", "start_char": 0, "end_char": 537, "text_sha256": "2a31ba5c71ba785b8fc6cdec21ed2dfa37686cb6d44dbf22616b0ab9b585a940"} [dim-p21599724] Effect of nicotine on cytochrome P450 1A2 activity. (2011). https://pubmed.ncbi.nlm.nih.gov/21599724/ DOI: 10.1111/j.1365-2125.2011.04023.x
Complete structured claim and evidenceCaffeine clearance fell by 36.1% after cessation; the fitted half-life of CYP1A2 activity decline was 38.6 hours.
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
- Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking.
- 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 844–855
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-smoking-cessation Caffeine clearance fell by 36.1% after cessation; the fitted half-life of CYP1A2 activity decline was 38.6 hours. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: Stopping an established inducer can raise exposure to its substrates, but these numbers describe smoking. 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 evidenceMedian caffeine clearance fell from 107 to 21 mL/min during fluvoxamine treatment.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers.
- limitations
- Study used 200 mg caffeine and repeated fluvoxamine; not a prediction of the same effect size for every CYP1A2 inhibitor.
- nutrient_topic
- Caffeine collection; salts, coffee, species and coexposure contexts retain their identities. · Caffeine
- plain_language
- Inhibiting the metabolic pathway slowed caffeine removal.
- 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 196–202
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-fluvox-clear Inhibiting the metabolic pathway slowed caffeine removal. Median caffeine clearance fell from 107 to 21 mL/min during fluvoxamine treatment. Model: Human caffeine/fluvoxamine crossover and metabolite measurements; eight healthy volunteers. Limitations: Study used 200 mg caffeine and repeated fluvoxamine; not a prediction of the same effect size for every CYP1A2 inhibitor. 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
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.