Component
Serum TSH concentration
Independent biological entity. Read linked claims for experimental scope and context.
7 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
T4 suppressed serum TSH in hypothyroid wild-type mice but not Dio2-null mice; administered T3 suppressed TSH in both genotypes.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- cross_nutrient
- Selenoenzyme D2 activates an iodine-containing hormone for feedback; knockout is a machinery experiment.
- evidence_locator
- Results: TSH Suppression Studies and Figure 9; pages 2140–2141.
- evidence_spans
- [{"source_document": "artifacts/iodine-metabolism-sources/11731615.txt", "locator": "Primary article Results, Figures 7 and 9; Methods: Assays for Serum T4, T3 and TSH, page 2146", "start_char": 20490, "end_char": 22790}]
- experimental_model
- Dio2-null mice and wild-type littermates, including hormone challenge after hypothyroidism
- exposure
- Male mice made hypothyroid for four weeks with methimazole/perchlorate; PTU inhibited D1. Subcutaneous T4 3 micrograms/100 g body weight or T3 1.2 micrograms/100 g; serum collected five hours later.
- limitations
- Pharmacologic hormone challenge after thyroid synthesis blockade and D1 inhibition; not a human dosing rule or dietary selenium-deficiency experiment.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Mus musculus
- plain_language
- T3 bypassed the missing local T4-activation step in this feedback experiment.
- primary_references
- [i-met-11731615] Targeted disruption of the type 2 selenodeiodinase gene (DIO2) results in a phenotype of pituitary resistance to T4. (2001). https://pubmed.ncbi.nlm.nih.gov/11731615/ DOI: 10.1210/mend.15.12.0740
- tissue_or_cell_type
- Pituitary feedback and serum TSH
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1025–1038
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dio2-null mice and wild-type littermates, including hormone challenge after hypothyroidism · source_derived_draft · unverified_draft
### i-met-dio2-t4-feedback T4 suppressed serum TSH in hypothyroid wild-type mice but not Dio2-null mice; administered T3 suppressed TSH in both genotypes. Condition category: machinery_impairment nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: T3 bypassed the missing local T4-activation step in this feedback experiment. organism: Mus musculus tissue_or_cell_type: Pituitary feedback and serum TSH experimental_model: Dio2-null mice and wild-type littermates, including hormone challenge after hypothyroidism limitations: Pharmacologic hormone challenge after thyroid synthesis blockade and D1 inhibition; not a human dosing rule or dietary selenium-deficiency experiment. exposure: Male mice made hypothyroid for four weeks with methimazole/perchlorate; PTU inhibited D1. Subcutaneous T4 3 micrograms/100 g body weight or T3 1.2 micrograms/100 g; serum collected five hours later. cross_nutrient: Selenoenzyme D2 activates an iodine-containing hormone for feedback; knockout is a machinery experiment. evidence_locator: Results: TSH Suppression Studies and Figure 9; pages 2140–2141. evidence_spans: [{"source_document": "artifacts/iodine-metabolism-sources/11731615.txt", "locator": "Primary article Results, Figures 7 and 9; Methods: Assays for Serum T4, T3 and TSH, page 2146", "start_char": 20490, "end_char": 22790}] [i-met-11731615] Targeted disruption of the type 2 selenodeiodinase gene (DIO2) results in a phenotype of pituitary resistance to T4. (2001). https://pubmed.ncbi.nlm.nih.gov/11731615/ DOI: 10.1210/mend.15.12.0740
Complete structured claim and evidenceAll iodide-supplemented groups had significant increases in TSH and median urinary iodine relative to placebo after four weeks (P<0.05).
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary indexed abstract.
- experimental_model
- Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults
- exposure
- Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day.
- limitations
- Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. Baseline participants were euthyroid; increased TSH alone does not identify the molecular inhibition step.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens
- plain_language
- More iodine raised TSH in this short dose-ranging trial.
- primary_references
- [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001
- tissue_or_cell_type
- Serum thyroid indices, ultrasound and urinary iodine
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1454–1466
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults · source_derived_draft · unverified_draft
### iod-clin-excess-tsh All iodide-supplemented groups had significant increases in TSH and median urinary iodine relative to placebo after four weeks (P<0.05). Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: More iodine raised TSH in this short dose-ranging trial. organism: Homo sapiens tissue_or_cell_type: Serum thyroid indices, ultrasound and urinary iodine experimental_model: Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults limitations: Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. Baseline participants were euthyroid; increased TSH alone does not identify the molecular inhibition step. exposure: Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day. cross_nutrient: false evidence_location: Primary indexed abstract. [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001
Complete structured claim and evidenceVitamin A without iodine supplementation lowered TSH in the iodine-deficient study setting.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- Vitamin A/iodine -> thyroid feedback.
- experimental_model
- 404 children; factorial trial.
- limitations
- TSH-beta transcriptional suppression is an explanation, not a directly measured step in these children.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Vitamin A status affected how strongly the thyroid was being stimulated.
- primary_references
- [va-zimmermann2007-iodine] Vitamin A supplementation in iodine-deficient African children decreases thyrotropin stimulation of the thyroid and reduces the goiter rate (2007). https://pubmed.ncbi.nlm.nih.gov/17921382/ DOI: 10.1093/ajcn/86.4.1040
- tissue_or_cell_type
- Pituitary-thyroid axis
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1578–1588
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 404 children; factorial trial. · source_derived_draft · unverified_draft
### va-iodine-context-lowers-tsh Vitamin A without iodine supplementation lowered TSH in the iodine-deficient study setting. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A status affected how strongly the thyroid was being stimulated. organism: Homo sapiens tissue_or_cell_type: Pituitary-thyroid axis experimental_model: 404 children; factorial trial. limitations: TSH-beta transcriptional suppression is an explanation, not a directly measured step in these children. cross_nutrient: Vitamin A/iodine -> thyroid feedback. [va-zimmermann2007-iodine] Vitamin A supplementation in iodine-deficient African children decreases thyrotropin stimulation of the thyroid and reduces the goiter rate (2007). https://pubmed.ncbi.nlm.nih.gov/17921382/ DOI: 10.1093/ajcn/86.4.1040
Complete structured claim and evidenceTSH fell from baseline in the myo-inositol-plus-selenomethionine arm, while no TSH change was reported in the selenomethionine-only arm; the reported TSH P value was a within-group comparison.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/24224112.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b9b55ed122a2f26149680eb0f4bfab9ea981927754bcbb40305d4697c5d32412", "start_char": 7984, "end_char": 8184, "text_sha256": "34e1c5b3fe451ea1278c2adfb27f4977a40d100b82946252ecad03a7879592dc"}
- experimental_model
- Double-blind randomized combination trial
- exposure
- Myo-inositol plus selenomethionine versus selenomethionine
- limitations
- Small combination trial without a myo-inositol-only arm. A significant within-group change versus a nonsignificant change in the other arm is not by itself a significant between-group difference or nutrient synergy.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- A thyroid blood marker improved in the combined-treatment group, but these comparisons do not establish a statistical interaction between nutrients.
- primary_references
- [ino-p24224112] Combined treatment with Myo-inositol and selenium ensures euthyroidism in subclinical hypothyroidism patients with autoimmune thyroiditis. (2013). https://pubmed.ncbi.nlm.nih.gov/24224112/ DOI: 10.1155/2013/424163
- tissue_or_cell_type
- Women with autoimmune subclinical hypothyroidism
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 1419–1430
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized combination trial · source_derived_draft · unverified_draft
### ino-thyroid-combination TSH fell from baseline in the myo-inositol-plus-selenomethionine arm, while no TSH change was reported in the selenomethionine-only arm; the reported TSH P value was a within-group comparison. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: A thyroid blood marker improved in the combined-treatment group, but these comparisons do not establish a statistical interaction between nutrients. organism: Homo sapiens tissue_or_cell_type: Women with autoimmune subclinical hypothyroidism experimental_model: Double-blind randomized combination trial limitations: Small combination trial without a myo-inositol-only arm. A significant within-group change versus a nonsignificant change in the other arm is not by itself a significant between-group difference or nutrient synergy. exposure: Myo-inositol plus selenomethionine versus selenomethionine evidence_span: {"source_cache": "artifacts/inositol-research/24224112.fulltext.txt", "locator": "Exact primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "b9b55ed122a2f26149680eb0f4bfab9ea981927754bcbb40305d4697c5d32412", "start_char": 7984, "end_char": 8184, "text_sha256": "34e1c5b3fe451ea1278c2adfb27f4977a40d100b82946252ecad03a7879592dc"} [ino-p24224112] Combined treatment with Myo-inositol and selenium ensures euthyroidism in subclinical hypothyroidism patients with autoimmune thyroiditis. (2013). https://pubmed.ncbi.nlm.nih.gov/24224112/ DOI: 10.1155/2013/424163
Complete structured claim and evidence
Where it participates (unsigned role)
Subclinical hypothyroidism occurred in 5% of the 400-microgram/day supplement group and 15–47% of the 500–2000-microgram/day groups.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary indexed abstract.
- experimental_model
- Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults
- exposure
- Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day.
- limitations
- Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. These percentages are reported study-group findings, not an individual risk calculator. The authors estimated about 800 micrograms/day total intake in the 400-microgram supplement group; adding two overall mean background values is not a group-specific intake measurement.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens
- plain_language
- Higher iodine exposure produced abnormal thyroid-function classifications in some participants.
- primary_references
- [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001
- tissue_or_cell_type
- Serum thyroid indices, ultrasound and urinary iodine
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1468–1480
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults · source_derived_draft · unverified_draft
### iod-clin-excess-subclinical Subclinical hypothyroidism occurred in 5% of the 400-microgram/day supplement group and 15–47% of the 500–2000-microgram/day groups. Condition category: normal nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Higher iodine exposure produced abnormal thyroid-function classifications in some participants. organism: Homo sapiens tissue_or_cell_type: Serum thyroid indices, ultrasound and urinary iodine experimental_model: Four-week randomized double-blind placebo-controlled dose trial in 256 euthyroid Chinese adults limitations: Short study with small dose groups. Total background iodine differs among participants; the approximately 800 micrograms/day total at the 400-microgram supplement is the authors’ estimate, not a universal safe/unsafe threshold. Exact chemical formulation not verified from abstract. These percentages are reported study-group findings, not an individual risk calculator. The authors estimated about 800 micrograms/day total intake in the 400-microgram supplement group; adding two overall mean background values is not a group-specific intake measurement. exposure: Twelve groups received 0–2000 micrograms/day supplemental iodine. Mean reported dietary and salt iodine contributions were 105 ± 25 and 258 ± 101 micrograms/day. cross_nutrient: false evidence_location: Primary indexed abstract. [iod-clin-sang2012] Exploration of the safe upper level of iodine intake in euthyroid Chinese adults: a randomized double-blind trial. (2012). https://pubmed.ncbi.nlm.nih.gov/22205314/ DOI: 10.3945/ajcn.111.028001
Complete structured claim and evidenceInfant thyroid hypofunction classifications were less frequent with indirect maternal supplementation (P=0.023), although infant TSH and T4 concentrations did not differ significantly between groups over time (P=0.597 and 0.184).
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- false
- evidence_location
- Primary PDF Methods, trial profile, Results and Table2, pp.197–209.
- experimental_model
- Double-blind randomized trial in Morocco;241 mother–infant pairs enrolled, 239 randomized after two age exclusions
- exposure
- Term infants ≤ 8 weeks; indirect arm 121 pairs: mother 400 mg iodine as oral iodized poppyseed oil, infant placebo; direct arm 118 pairs: infant about 100 mg iodine from half a 200 mg oil capsule, mother placebo; follow-up 3, 6, 9 months.
- limitations
- Both arms received active iodine somewhere in the pair; there was no wholly untreated arm. Breastfeeding and baseline deficiency contextualize the result; measured iodine status is not a child cognitive outcome. Actual infant study dose was about 100 mg, not the 200 mg guideline discussed elsewhere in the paper. No serious adverse events were reported; this does not establish safety for other infant doses, preparations or settings.
- nutrient_topic
- Iodine research collection; topical membership is not evidence of a direct dietary effect. · Iodine
- organism
- Homo sapiens
- plain_language
- A categorical thyroid outcome improved even though average hormone comparisons were not significant.
- primary_references
- [iod-clin-bouhouch2014] Direct iodine supplementation of infants versus supplementation of their breastfeeding mothers: a double-blind, randomised, placebo-controlled trial. (2014). https://pubmed.ncbi.nlm.nih.gov/24622750/ DOI: 10.1016/s2213-8587(13)70155-4
- tissue_or_cell_type
- Breast milk, infant urine and thyroid function
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Iodine: thyroid hormone production, deficiency, excess and nutrient interactions (2026-09-17) · lines 1566–1578
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized trial in Morocco;241 mother–infant pairs enrolled, 239 randomized after two age exclusions · source_derived_draft · unverified_draft
### iod-clin-lactation-hypofunction Infant thyroid hypofunction classifications were less frequent with indirect maternal supplementation (P=0.023), although infant TSH and T4 concentrations did not differ significantly between groups over time (P=0.597 and 0.184). Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A categorical thyroid outcome improved even though average hormone comparisons were not significant. organism: Homo sapiens tissue_or_cell_type: Breast milk, infant urine and thyroid function experimental_model: Double-blind randomized trial in Morocco;241 mother–infant pairs enrolled, 239 randomized after two age exclusions limitations: Both arms received active iodine somewhere in the pair; there was no wholly untreated arm. Breastfeeding and baseline deficiency contextualize the result; measured iodine status is not a child cognitive outcome. Actual infant study dose was about 100 mg, not the 200 mg guideline discussed elsewhere in the paper. No serious adverse events were reported; this does not establish safety for other infant doses, preparations or settings. exposure: Term infants ≤ 8 weeks; indirect arm 121 pairs: mother 400 mg iodine as oral iodized poppyseed oil, infant placebo; direct arm 118 pairs: infant about 100 mg iodine from half a 200 mg oil capsule, mother placebo; follow-up 3, 6, 9 months. cross_nutrient: false evidence_location: Primary PDF Methods, trial profile, Results and Table2, pp.197–209. [iod-clin-bouhouch2014] Direct iodine supplementation of infants versus supplementation of their breastfeeding mothers: a double-blind, randomised, placebo-controlled trial. (2014). https://pubmed.ncbi.nlm.nih.gov/24622750/ DOI: 10.1016/s2213-8587(13)70155-4
Complete structured claim and evidenceMean reverse T3 fell from 124 ± 115 to 90 ± 72 pmol/L after selenium treatment (P<0.05), while serum T3 and TSH did not change significantly.
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 hormone pattern changed unevenly; T3 and TSH did not simply rise with selenium.
- 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 1286–1298
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-rt3 Mean reverse T3 fell from 124 ± 115 to 90 ± 72 pmol/L after selenium treatment (P<0.05), while serum T3 and TSH did not change significantly. Condition category: nutrient_deficiency nutrient_topic: Iodine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone pattern changed unevenly; T3 and TSH did not simply rise with selenium. 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.