Component

Carbamazepine

Carbamazepine. 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. Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport.

    Carbamazepine → Cellular biotin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"}
    experimental_model
    Transport assays in purified human intestinal brush-border and basolateral membrane vesicles
    exposure
    Carbamazepine or primidone; millimolar inhibitor constants
    limitations
    These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient.
    nutrient_topic
    Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
    organism
    Homo sapiens
    plain_language
    The drug competed with biotin at the gut-facing membrane in this experiment.
    primary_references
    [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    tissue_or_cell_type
    Intestinal membrane vesicles
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 273–284

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport assays in purified human intestinal brush-border and basolateral membrane vesicles · source_derived_draft · unverified_draft

    ### b7-carbamazepine-uptake Carbamazepine competitively inhibited biotin uptake in human intestinal brush-border vesicles (Ki 4.70 mmol/L), without inhibiting basolateral biotin transport. Condition category: machinery_impairment nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug competed with biotin at the gut-facing membrane in this experiment. organism: Homo sapiens tissue_or_cell_type: Intestinal membrane vesicles experimental_model: Transport assays in purified human intestinal brush-border and basolateral membrane vesicles limitations: These are membrane-assay concentrations. The study does not establish that prescribed doses cause deficiency in every patient. exposure: Carbamazepine or primidone; millimolar inhibitor constants evidence_span: {"source_cache": "artifacts/biotin-research/2911998.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb", "start_char": 0, "end_char": 1045, "text_sha256": "15113710724eaa76fd9bee5cdf7b031ce185b922c826e10d27aa42235a17aeeb"} [b7-p2911998] Biotin transport in the human intestine: inhibition by anticonvulsant drugs. (1989). https://pubmed.ncbi.nlm.nih.gov/2911998/ DOI: 10.1093/ajcn/49.1.127
    Complete structured claim and evidence

  2. The carbamazepine/phenytoin group had higher urinary 3-HIA, but only one child in that group had low urinary biotin.

    Carbamazepine → Human urinary 3-hydroxyisovaleric acid excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"}
    experimental_model
    Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls
    exposure
    Long-term anticonvulsant treatment
    limitations
    Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis.
    nutrient_topic
    Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
    organism
    Homo sapiens
    plain_language
    Different biotin-status markers did not give the same answer in these children.
    primary_references
    [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
    tissue_or_cell_type
    Urine
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 312–323

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls · source_derived_draft · unverified_draft

    ### b7-drug-3hia The carbamazepine/phenytoin group had higher urinary 3-HIA, but only one child in that group had low urinary biotin. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Different biotin-status markers did not give the same answer in these children. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls limitations: Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis. exposure: Long-term anticonvulsant treatment evidence_span: {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"} [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
    Complete structured claim and evidence

  3. Urinary bisnorbiotin was higher in both carbamazepine/phenytoin-treated and phenobarbital-treated children than in controls.

    Carbamazepine → Human urinary bisnorbiotin excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"}
    experimental_model
    Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls
    exposure
    Long-term anticonvulsant treatment
    limitations
    Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis.
    nutrient_topic
    Biotin research collection; topical membership is not evidence of a direct dietary effect. · Biotin
    organism
    Homo sapiens
    plain_language
    Some anticonvulsant-treated children excreted more of a biotin breakdown product.
    primary_references
    [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
    tissue_or_cell_type
    Urine
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Biotin: carboxylases, recycling, deficiency and nutrient interactions (2026-09-17) · lines 299–310

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls · source_derived_draft · unverified_draft

    ### b7-drug-bisnorbiotin Urinary bisnorbiotin was higher in both carbamazepine/phenytoin-treated and phenobarbital-treated children than in controls. Condition category: biomarker_context nutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some anticonvulsant-treated children excreted more of a biotin breakdown product. organism: Homo sapiens tissue_or_cell_type: Urine experimental_model: Observational urine comparison: 7 children receiving carbamazepine/phenytoin, 6 phenobarbital, 16 controls limitations: Untimed urine, small nonrandomized groups and discordant markers limit diagnosis; faster turnover is not a universal deficiency diagnosis. exposure: Long-term anticonvulsant treatment evidence_span: {"source_cache": "artifacts/biotin-research/9523856.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136", "start_char": 0, "end_char": 1876, "text_sha256": "a337d853fbf3d26e053dfd6d17b2e1729c993a0501563d0524ebbee7b44d5136"} [b7-p9523856] Disturbances in biotin metabolism in children undergoing long-term anticonvulsant therapy. (1998). https://pubmed.ncbi.nlm.nih.gov/9523856/ DOI: 10.1097/00005176-199803000-00002
    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