Component

Nicotine

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

4 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.

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. Nicotine patches did not significantly change caffeine pharmacokinetics or metabolite formation in the crossover study.

    Nicotine → Caffeine clearance source_derived_draftungraded
    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 evidence
  2. Nicotine inhibited CYP2A6 coumarin hydroxylation within the study inhibitor category of Ki below 200 micromolar.

    Nicotine → Coumarin 7-hydroxylation source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/coumarin-research/9143352.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09", "start_char": 0, "end_char": 2723, "text_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09"}
    experimental_model
    Human microsomal and recombinant CYP2A6 inhibitor screen
    exposure
    Coumarin 0.5–50 micromolar; 47 inhibitor/substrate probes
    limitations
    In vitro inhibition thresholds are not demonstrated clinical interactions at food exposure.
    nutrient_topic
    Coumarin research collection; topical membership is not evidence of a direct dietary effect. · Coumarin
    organism
    Human
    plain_language
    Nicotine and coumarin can interact in an enzyme assay.
    primary_references
    [coumarin-p9143352] Inhibition of coumarin 7-hydroxylase activity in human liver microsomes. (1997). https://pubmed.ncbi.nlm.nih.gov/9143352/ DOI: 10.1006/abbi.1997.9964
    tissue_or_cell_type
    Liver enzyme preparations

    Coumarin: metabolism, signaling and nutrient connections (2026-09-17) · lines 579–590

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human microsomal and recombinant CYP2A6 inhibitor screen · source_derived_draft · unverified_draft

    ### coumarin-nicotine-inhibition Nicotine inhibited CYP2A6 coumarin hydroxylation within the study inhibitor category of Ki below 200 micromolar. Condition category: normal nutrient_topic: Coumarin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotine and coumarin can interact in an enzyme assay. organism: Human tissue_or_cell_type: Liver enzyme preparations experimental_model: Human microsomal and recombinant CYP2A6 inhibitor screen limitations: In vitro inhibition thresholds are not demonstrated clinical interactions at food exposure. exposure: Coumarin 0.5–50 micromolar; 47 inhibitor/substrate probes evidence_span: {"source_cache": "artifacts/coumarin-research/9143352.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09", "start_char": 0, "end_char": 2723, "text_sha256": "dca3f4253c2977d47070bb95696634ee2e06fa9a28a3d76ac9790ce695ed6f09"} [coumarin-p9143352] Inhibition of coumarin 7-hydroxylase activity in human liver microsomes. (1997). https://pubmed.ncbi.nlm.nih.gov/9143352/ DOI: 10.1006/abbi.1997.9964
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The clinical trial found no significant nicotine AUC change with the characterized C. verum regimen; the geometric mean exposure ratio was 0.98.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/41622703.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0d12141499aba319f8c7513f708889a4dc40fae628e26600f780be2323fe0db3", "start_char": 0, "end_char": 1643, "text_sha256": "0d12141499aba319f8c7513f708889a4dc40fae628e26600f780be2323fe0db3"}
    experimental_model
    Within-person clinical pharmacokinetic comparison
    exposure
    Characterized C. verum 2 g three times daily for five days, with day-six drug coadministration and two further cinnamon doses; nicotine gum 2 mg or letrozole 2.5 mg
    limitations
    Product- and regimen-specific short-term result, not proof of no interaction with all drugs, oils or extracts. CYP2A6 model predictions did not translate into large AUC changes here.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human
    plain_language
    The large interaction predicted from enzyme models was not seen for nicotine in this human study.
    primary_references
    [ceylon-p41622703] Pharmacokinetic Evaluation of a Cinnamon Product on CYP2A6 Substrate Drugs: Application of a Novel Tool Involving the Nicotine Metabolite Ratio. (2026). https://pubmed.ncbi.nlm.nih.gov/41622703/ DOI: 10.1002/cpt.70218
    tissue_or_cell_type
    16 healthy non-nicotine-using adults; plasma drug profiles

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 1195–1206

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Within-person clinical pharmacokinetic comparison · source_derived_draft · unverified_draft

    ### ceylon-nicotine-clinical The clinical trial found no significant nicotine AUC change with the characterized C. verum regimen; the geometric mean exposure ratio was 0.98. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: The large interaction predicted from enzyme models was not seen for nicotine in this human study. organism: Human tissue_or_cell_type: 16 healthy non-nicotine-using adults; plasma drug profiles experimental_model: Within-person clinical pharmacokinetic comparison limitations: Product- and regimen-specific short-term result, not proof of no interaction with all drugs, oils or extracts. CYP2A6 model predictions did not translate into large AUC changes here. exposure: Characterized C. verum 2 g three times daily for five days, with day-six drug coadministration and two further cinnamon doses; nicotine gum 2 mg or letrozole 2.5 mg evidence_span: {"source_cache": "artifacts/ceylon-research/41622703.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0d12141499aba319f8c7513f708889a4dc40fae628e26600f780be2323fe0db3", "start_char": 0, "end_char": 1643, "text_sha256": "0d12141499aba319f8c7513f708889a4dc40fae628e26600f780be2323fe0db3"} [ceylon-p41622703] Pharmacokinetic Evaluation of a Cinnamon Product on CYP2A6 Substrate Drugs: Application of a Novel Tool Involving the Nicotine Metabolite Ratio. (2026). https://pubmed.ncbi.nlm.nih.gov/41622703/ DOI: 10.1002/cpt.70218
    Complete structured claim and evidence
  2. The rat-scaled static model predicted a 4.29-fold nicotine AUC with the modeled cinnamaldehyde exposure.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ceylon-research/32788161.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "431169f83241cb83b84dd81d84eb1db225735677cabf33f09af8b1e22dfe64f4", "start_char": 0, "end_char": 2507, "text_sha256": "431169f83241cb83b84dd81d84eb1db225735677cabf33f09af8b1e22dfe64f4"}
    experimental_model
    CYP2A6 mass spectrometry, time-dependent inhibition and numerical modeling
    exposure
    Cinnamaldehyde and separately 2-methoxycinnamaldehyde; model exposure approximately 275 mg cinnamaldehyde
    limitations
    Rat-scaled predicted human AUC is not observed AUC. Heme loss was specifically reported for the methoxy analogue; apoprotein adduction is a different endpoint from inhibition.
    nutrient_topic
    Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. · Ceylon cinnamon / Cinnamomum verum bark preparations
    organism
    Human CYP2A6; rat-scaled modeling parameters
    plain_language
    This was a forecast from enzyme data and assumptions, not a result in people.
    primary_references
    [ceylon-p32788161] Mechanisms of Herb-Drug Interactions Involving Cinnamon and CYP2A6: Focus on Time-Dependent Inhibition by Cinnamaldehyde and 2-Methoxycinnamaldehyde. (2020). https://pubmed.ncbi.nlm.nih.gov/32788161/ DOI: 10.1124/dmd.120.000087
    tissue_or_cell_type
    Enzyme apoprotein/heme; simulated drug exposure

    Ceylon cinnamon: metabolism, signaling and nutrient connections (2026-09-17) · lines 792–803

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CYP2A6 mass spectrometry, time-dependent inhibition and numerical modeling · source_derived_draft · unverified_draft

    ### ceylon-predicted-nicotine The rat-scaled static model predicted a 4.29-fold nicotine AUC with the modeled cinnamaldehyde exposure. Condition category: normal nutrient_topic: Ceylon cinnamon research collection; topical membership is not evidence of a direct dietary effect. plain_language: This was a forecast from enzyme data and assumptions, not a result in people. organism: Human CYP2A6; rat-scaled modeling parameters tissue_or_cell_type: Enzyme apoprotein/heme; simulated drug exposure experimental_model: CYP2A6 mass spectrometry, time-dependent inhibition and numerical modeling limitations: Rat-scaled predicted human AUC is not observed AUC. Heme loss was specifically reported for the methoxy analogue; apoprotein adduction is a different endpoint from inhibition. exposure: Cinnamaldehyde and separately 2-methoxycinnamaldehyde; model exposure approximately 275 mg cinnamaldehyde evidence_span: {"source_cache": "artifacts/ceylon-research/32788161.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "431169f83241cb83b84dd81d84eb1db225735677cabf33f09af8b1e22dfe64f4", "start_char": 0, "end_char": 2507, "text_sha256": "431169f83241cb83b84dd81d84eb1db225735677cabf33f09af8b1e22dfe64f4"} [ceylon-p32788161] Mechanisms of Herb-Drug Interactions Involving Cinnamon and CYP2A6: Focus on Time-Dependent Inhibition by Cinnamaldehyde and 2-Methoxycinnamaldehyde. (2020). https://pubmed.ncbi.nlm.nih.gov/32788161/ DOI: 10.1124/dmd.120.000087
    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