Component
Serum free thyroxine concentration
Serum free thyroxine concentration. Study-specific scope and measurement methods are recorded with each 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
With MMI 15 mg, two-week FT4 normalization was 54% with KI versus 27% without it.
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- 134 untreated Graves patients randomized to MMI 15 or 30 mg, with or without KI; KI withdrawn after FT4 normalization.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 evidenceAt two weeks, FT4 normalized in 59% with MMI 30 mg plus KI versus 29% with MMI alone.
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 evidenceMean serum free T4 fell from 11.8 ± 6.7 to 8.4 ± 4.1 pmol/L after selenium treatment (P<0.01).
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- true
- evidence_location
- Primary indexed abstract.
- experimental_model
- Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire
- exposure
- Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract.
- limitations
- The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens
- plain_language
- The free T4 measurement also fell after selenium was added.
- primary_references
- [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x
- tissue_or_cell_type
- Serum thyroid-hormone concentrations
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1272–1284
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire · source_derived_draft · unverified_draft
### iod-clin-selenium-free-t4 Mean serum free T4 fell from 11.8 ± 6.7 to 8.4 ± 4.1 pmol/L after selenium treatment (P<0.01). Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The free T4 measurement also fell after selenium was added. organism: Homo sapiens tissue_or_cell_type: Serum thyroid-hormone concentrations experimental_model: Placebo-controlled selenium intervention in 52 schoolchildren from a region of severe iodine and selenium deficiency in northern Zaire limitations: The abstract reports before/after changes in the selenium group; do not mistake these for adjusted between-group estimates. DIO1 restoration was a proposed explanation, not directly measured. Hormone changes do not themselves establish symptomatic deterioration or a universal order for supplement treatment. exposure: Selenium 50 micrograms/day as selenomethionine or placebo for two months; no concurrent iodine-repletion regimen reported in the abstract. cross_nutrient: true evidence_location: Primary indexed abstract. [iod-clin-contempre1992] Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population. (1992). https://pubmed.ncbi.nlm.nih.gov/1424183/ DOI: 10.1111/j.1365-2265.1992.tb02268.x
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.