Component

Methimazole

Methimazole

5 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. Methimazole suppressed the inhibitory effects of iodide on stimulated H2O2 generation in dog thyroid slices.

    Methimazole → Iodide induced peroxide inhibition source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_span
    {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."}
    experimental_model
    Dog thyroid slices with iodide, stimulatory probes and methimazole
    exposure
    Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract. Methimazole coexposure.
    limitations
    Pharmacological probe supports oxidation dependence; the inhibitory iodinated species was not identified.
    nutrient_topic
    Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
    organism
    Canis lupus familiaris
    plain_language
    Preventing iodide oxidation blocked this feedback effect in thyroid tissue.
    primary_references
    [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3
    tissue_or_cell_type
    Thyroid slices

    Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 814–826

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dog thyroid slices with iodide, stimulatory probes and methimazole · source_derived_draft · unverified_draft

    ### iodine-syn-acute-block-oxidation Methimazole suppressed the inhibitory effects of iodide on stimulated H2O2 generation in dog thyroid slices. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Preventing iodide oxidation blocked this feedback effect in thyroid tissue. organism: Canis lupus familiaris tissue_or_cell_type: Thyroid slices experimental_model: Dog thyroid slices with iodide, stimulatory probes and methimazole limitations: Pharmacological probe supports oxidation dependence; the inhibitory iodinated species was not identified. exposure: Iodide exposure in dog thyroid slices stimulated by thyrotropin, carbamylcholine or intracellular-signaling probes; concentrations not given in abstract. Methimazole coexposure. cross_nutrient: false evidence_span: {"source_cache": "artifacts/iodine-synthesis-sources/2841932.json", "json_field": "abstractText", "text_sha256": "00e19301656f8e8fdb9a047cfa29daf1c66f9a73c84d6c450ff805a6d8b497eb", "text_characters": 1113, "note": "Exact publisher passage retained in the cited local source cache; locator and digest supplied here."} [iodine-syn-block1988] Inhibition by iodide of iodide binding to proteins: the "Wolff-Chaikoff" effect is caused by inhibition of H2O2 generation. (1988). https://pubmed.ncbi.nlm.nih.gov/2841932/ DOI: 10.1016/0006-291x(88)90279-3
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The label warns that lithium or antithyroid drugs can add to hypothyroid and goitrogenic effects.

    Potassium iodide → Goitrous hypothyroidism source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    2025 SSKI manufacturer label; 1 g KI/mL formulation.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    Different drugs can converge on reduced thyroid function.
    primary_references
    SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 456–462

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 2025 SSKI manufacturer label; 1 g KI/mL formulation. · source_derived_draft · unverified_draft

    ## ki-lithium Different drugs can converge on reduced thyroid function. The label warns that lithium or antithyroid drugs can add to hypothyroid and goitrogenic effects. Model: 2025 SSKI manufacturer label; 1 g KI/mL formulation. Limitations: Label warning, not a quantified primary interaction trial; applicability depends on exposure and patient context. Evidence location: Primary abstract SSKI product label, July 2025 · manufacturer label; DailyMed lists UNAPPROVED DRUG OTHER; not a trial or FDA approval · https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=ca1d3449-ea29-49a4-8863-365ec95f1553
    Complete structured claim and evidence

  2. With MMI 15 mg, two-week FT4 normalization was 54% with KI versus 27% without it.

    Potassium iodide → Serum free thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    The lower-methimazole comparison also showed faster control.
    primary_references
    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 392–398

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-mmi15 The lower-methimazole comparison also showed faster control. With MMI 15 mg, two-week FT4 normalization was 54% with KI versus 27% without it. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x
    Complete structured claim and evidence

  3. At two weeks, FT4 normalized in 59% with MMI 30 mg plus KI versus 29% with MMI alone.

    Potassium iodide → Serum free thyroxine concentration source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    KI accelerated early control alongside methimazole.
    primary_references
    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 384–390

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-mmi30 KI accelerated early control alongside methimazole. At two weeks, FT4 normalized in 59% with MMI 30 mg plus KI versus 29% with MMI alone. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x
    Complete structured claim and evidence

  4. Remission differences between the four regimens were not statistically significant at four to five years.

    Potassium iodide → Graves disease remission in the specified study source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.
    exposure_category
    Study-specific exposure, including pharmacological and in-vitro conditions; normal is the schema fallback outside the three availability categories.
    limitations
    Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission.
    nutrient_topic
    Potassium iodide research collection; shared-anion and comparator studies are not all KI interventions. · Potassium iodide
    plain_language
    Early hormone improvement did not establish a remission advantage.
    primary_references
    Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.x

    Potassium iodide: thyroid and non-thyroid mechanisms, interactions and discovery questions (2026-09-18) · lines 400–406

    AI-assisted research curation; primary-study references, chemical references and label statements individually identified. Not publisher full text. · supports · 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. · source_derived_draft · unverified_draft

    ## ki-remission-null Early hormone improvement did not establish a remission advantage. Remission differences between the four regimens were not statistically significant at four to five years. Model: 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization. Limitations: Combination treatment, not KI monotherapy; KI dose not extracted from abstract. Faster biochemical control does not prove lasting remission. Evidence location: Primary abstract Benefit of short-term iodide supplementation to antithyroid drug treatment of thyrotoxicosis due to Graves' disease. · 2010 · https://pubmed.ncbi.nlm.nih.gov/19912243/ · DOI 10.1111/j.1365-2265.2009.03745.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.

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