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MyDeficiencies

Potassium iodide

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Findings for this medication

Research about this medication, graded for how strongly each finding can be attributed to it. Nothing here describes your own levels.

Potassium iodide is an inorganic ionic salt, not a conventional xenobiotic: neither its SSKI nor its ThyroShield FDA label describes hepatic CYP450 metabolism, enzyme induction or inhibition. Absorbed iodide is either taken up by thyroid follicular cells through the sodium-iodide symporter and organified onto thyroglobulin, or excreted largely unchanged by the kidney, aided by "abundant fluid and salt intake" per the SSKI label. Because the drug's entire pharmacology is delivering iodide, and because it is dosed as a potassium salt, this dossier's dominant, best-documented findings are two excess/retention entries rather than classical depletion mechanisms: iodine/thyroid hormone status itself, and the potassium counter-ion. A 300-600 mg SSKI dose delivers roughly 1.8-3.6 mEq of elemental potassium (derived from potassium iodide's molecular weight, 39.10/166.00 = 23.6% potassium by mass; not a cited study figure), on top of whatever potassium the patient's diet, renal function and other medications already carry.

ATC R05CA02 (expectorant, primary WHO listing); V03AB21 (antidote / radioprotective) ยท also sold as SSKI (Avondale) and ThyroShield (Fleming) and generic potassium iodide oral solution (Nivagen) ยท reviewed 2026-09-28. This describes research about the medication. It does not say anything about your own levels or health.

How to read the evidence grades

These colours describe how strongly a finding can be attributed to the medication in the research. They are not a severity score and they say nothing about your own health.

Grades describe how strongly a finding can be attributed to Potassium iodide in the research โ€” not how common it is, how serious it would be, and not anything about you personally.

Red โ€” Severe
Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence.
Orange โ€” Moderate
At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit.
Yellow โ€” Low
Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction.
Not graded โ€” disclosed evidence gap
Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result.Source definition: Not gradeable under the rules above because nothing has been measured. Published as a documented gap, never as reassurance that there is no effect.

What the research found

Iodine / thyroid hormone status, iodine-induced hypothyroidism and Jod-Basedow hyperthyroidism

Red โ€” Severe

See study details

Potassium iodide's own iodide load can push thyroid hormone synthesis in either direction: prolonged use can cause hypothyroidism (escape failure from the Wolff-Chaikoff block), while excess iodide in a susceptible nodular or autoimmune gland can trigger Jod-Basedow hyperthyroidism. This is an excess/retention risk from the drug's own chemistry, not an iodine deficiency, and the acute block itself is the intended, monitored effect in thyroid storm.

Full detail and limits

What the grade means here: Two or more independent Tier A sources, this drug in the cohort, the nutrient directly measured, consistent direction, clinically meaningful magnitude, a named mechanism, no substantial contradicting Tier A evidence. RED

Limits on what this shows

  • Key null/negative: None identified, this is an established, expected, and actively monitored bidirectional effect in the endocrine literature and on both labels, not a disputed one.
  • At-risk subgroups: Neonates and the fetus (both labels warn of fetal harm, abnormal thyroid function and goiter in pregnancy); patients with underlying autoimmune thyroiditis (hypothyroidism-escape-failure risk); patients with nodular thyroid disease or latent Graves' disease (Jod-Basedow risk); ThyroShield is separately contraindicated in nodular thyroid disease with concurrent cardiac disease.
  • Counter-evidence: None on record; direction (bidirectional dysfunction risk from iodide excess) is not contested in the sources reviewed. The acute suppression of thyroid hormone release is the intended, beneficial effect in thyroid storm and is not itself counter-evidence against the excess-risk framing of prolonged or unmonitored use.

Regulatory status

SSKI label: "prolonged use of iodides can lead to hypothyroidism." ThyroShield label, independently: "may cause overactivity, underactivity, or enlargement (goiter)" of the thyroid; neonates specifically flagged for hypothyroidism risk with recommended thyroid monitoring. Both are FDA-facing labels for potassium-iodide-containing products.

Population evidence

Two independent, drug-specific Tier A regulatory labels (SSKI, ThyroShield), each separately warning of thyroid dysfunction from this drug's iodide load, satisfy the โ‰ฅ2 independent Tier A source bar. Clinical use in thyroid storm and preoperative Graves' disease (deliberately exploiting the acute block) is separately documented in the endocrine literature (e.g. Yeung et al. 1995, Thyroid, rectal iodide plus propylthiouracil for thyroid storm; title/journal confirmed via Crossref, full text not independently opened this session, see Sources).

Mechanism

Acute Wolff-Chaikoff block: high intrathyroidal iodide transiently inhibits organification and hormone release. Most glands "escape" this block within days; failure to escape (more common in underlying autoimmune thyroiditis) produces hypothyroidism. Conversely, iodide oversupply to an autonomously functioning nodule or latent Graves' disease can precipitate iodine-induced (Jod-Basedow) hyperthyroidism.

Counter-evidence held on record

This is an excess/retention risk from the drug's own iodide chemistry, not an iodine deficiency, and must never be used to justify additional iodine or seaweed/kelp supplementation. During legitimate acute thyroid-storm or radiation-blocking use, dosing and duration should follow prescriber guidance and the monitoring schedule below; the concern applies chiefly to prolonged, unmonitored, or self-directed use.

Potassium, hyperkalemia risk with potassium-sparing agents or renal impairment

Orange โ€” Moderate

See study details

Each dose of potassium iodide delivers a real potassium load (roughly 1.8-3.6 mEq per 300-600 mg SSKI dose, by molecular weight), and the SSKI label directly warns that combining it with potassium-sparing agents may cause hyperkalemia and cardiac arrhythmia or arrest. This is a retention/excess risk, not a potassium deficiency, and is bounded here to one labeled Tier A source because a second independent drug-specific source could not be located.

Full detail and limits

What the grade means here: At least one Tier A source with this drug in the cohort showing a real but bounded deficit: an exposure window, a subgroup, low frequency, or a functional rather than circulating deficit. ORANGE

Limits on what this shows

  • Key null/negative: None identified; no study measuring serum potassium in patients on SSKI/ThyroShield without a potassium-sparing co-medication was located to confirm or refute a null baseline-dosing effect.
  • At-risk subgroups: Patients on potassium-sparing diuretics (spironolactone, eplerenone, amiloride, triamterene), ACE inhibitors or ARBs, or with renal impairment; higher, more frequent SSKI dosing regimens (up to 600 mg four times daily, roughly 14.4 mEq/day) carry a larger cumulative load than a single ThyroShield radiation-blocking dose (about 0.8 mEq/day at the adult dose).

Regulatory status

SSKI label, drug interactions: concurrent use with potassium-sparing agents "may result in hyperkalemia and cardiac arrhythmias or cardiac arrest." ThyroShield's label does not separately address drug interactions or potassium load.

Population evidence

Labeled warning only; no dedicated potassium-iodide-specific case series or cohort study of serum potassium was located after multiple Crossref queries ("potassium iodide hyperkalemia," "potassium iodide SSKI potassium salt load"). One adjacent case report was found and opened describing hyperkalemia from potassium-enriched table salt, not potassium iodide (Kusunoki et al. 2025, Cureus ), used only as Tier C context for plausibility of a real potassium salt load causing hyperkalemia in a hospitalized patient, not counted toward this drug's own tier.

Mechanism

Direct potassium salt load (1.8-3.6 mEq elemental potassium per 300-600 mg SSKI dose, derived from potassium iodide's 23.6%-by-mass potassium content; not a cited study figure), additive to dietary potassium and compounded by any concurrent impairment of renal or aldosterone-mediated potassium excretion (potassium-sparing diuretics, ACE inhibitors/ARBs by general pharmacologic mechanism, renal impairment).

Why not RED

Only one independent Tier A source (a single label's interaction warning) was located; no second Tier A source or drug-specific case-control/case-series study was found despite multiple search attempts across Crossref, PubMed and Europe PMC (the latter two blocked this session, see Sources access note). At a single unblocked 300-600 mg dose without a potassium-sparing co-medication, the added potassium load is small relative to typical daily intake.

Counter-evidence held on record

Excess/retention risk, not a potassium deficiency. Never a rationale for potassium supplementation; the concern runs toward reducing or avoiding concurrent potassium-sparing agents and monitoring serum potassium under a prescriber, particularly in renal impairment.

Selenium, reverse-direction interaction

Yellow โ€” Low

See study details

In a population with combined iodine and selenium deficiency, selenium repletion given without correcting iodine status worsened, rather than improved, thyroid function in already-hypothyroid subjects. This documents selenium status modifying the response to iodine/thyroid status, the reverse of potassium iodide affecting selenium levels, and is not potassium-iodide-specific.

Full detail, limits and 1 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. YELLOW

Limits on what this shows

  • Key null/negative: None identified for potassium-iodide-specific selenium status; no study measuring selenium or glutathione peroxidase levels before/after SSKI or ThyroShield dosing was located.

Population evidence

Contempre B, Dumont JE, Ngo B, Thilly CH, Diplock AT, Vanderpas J. J Clin Endocrinol Metab 1991;73(1):213-215 (PMID 2045471). Human supplementation study, northern Zaire, an area of combined endemic iodine and selenium deficiency; clinically euthyroid and clinically hypothyroid subjects. Two months of selenium supplementation normalized glutathione peroxidase activity and altered thyroid hormone parameters in euthyroid subjects, but produced "a dramatic fall of the already impaired thyroid function" in clinically hypothyroid subjects whose iodine deficiency was not simultaneously corrected.

Mechanism

Selenium-dependent glutathione peroxidase and deiodinase activity are part of normal thyroid hormone handling; correcting selenium deficiency alone, in a still-iodine-deficient gland, is proposed to accelerate thyroid failure rather than relieve it (consistent with the H2O2/fibrosis mechanism in the Oxidative stress entry's Contempre 2004 rat model).

Tier and direction

Tier A for the human finding, but the studied intervention is selenium supplementation in an iodine-deficient population, not potassium iodide administration in a selenium-deficient population; the direction is the reverse of a "drug depletes nutrient" claim. Graded yellow as a class-level/context-flag interaction per protocol, not as a depletion finding, and not elevated to orange/red because potassium iodide itself was not the studied intervention.

Overlap

Shares Contempre et al. 2004 (rat model) with the Oxidative stress entry above, see Overlap map. Do not read the two entries as independent confirmations of a single effect.

Counter-evidence held on record

This describes selenium status affecting thyroid tolerance of iodine level, not potassium iodide depleting selenium, and carries no implication that selenium supplementation should accompany potassium iodide dosing; the cited literature in fact cautions against selenium supplementation without first addressing iodine status. No dose is recommended.

The five body-system areas

Each finding is counted once, in a single area. Where a study is mentioned in a second area it is context only.

Mitochondrial Burden

Each finding below is counted once, in this area only.

Mitochondrial burden

Not graded โ€” disclosed evidence gap

See study details

No drug-specific or class-level evidence connects potassium iodide directly to mitochondrial structure, membrane integrity, electron transport or biogenesis, and no circulating consumer claim to rebut was found.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. UNGRADED

Limits on what this shows

  • Why no grade: Both UNGRADED conditions are met: (1) no Tier B/C evidence links potassium iodide, or iodide/iodine generally, to mitochondrial structure or function as a direct drug effect; (2) no circulating consumer claim naming potassium iodide and mitochondria was found in the sources checked. Thyroid hormone (T3) itself is well known in general endocrinology to regulate mitochondrial biogenesis, but that relationship runs through the drug's own intended pharmacologic target (thyroid hormone synthesis/release, which potassium iodide is used to suppress in thyroid storm) rather than being a direct nutrient-style mitochondrial effect of the drug; per Hard Rule 2, that downstream hormonal cascade is excluded here rather than filed as a mitochondrial finding.

Search channels tried, this revision (2026-09-28)

This category was genuinely re-searched, not carried forward. A PubMed search-listing query ("potassium iodide mitochondria") loaded successfully this time and returned 65 results across 7 pages; the 10 shown were opened and read in full, spanning potassium-channel pharmacology, unrelated mitochondrial toxicology, and organelle-motility papers, none connecting potassium iodide or iodide to mitochondrial structure or function. Two further Crossref API bibliographic queries ("iodide mitochondrial function cellular respiration"; a phrasing shared with the ATP production entry below) returned only Stat3-signaling and sex/age mitochondrial-atlas papers with no iodide relevance. The NIH Office of Dietary Supplements iodine health-professional fact sheet was opened and searched in full; it contains no mention of mitochondria. A follow-up, more targeted PubMed query and a Europe PMC query were both refused this session with an explicit do-not-retry HTTP 429 from the fetch proxy, and OpenAlex and Semantic Scholar queries returned HTTP 429 directly from the target servers; those channels were not force-retried per instruction. This is now a confirmed absence of Tier B/C evidence across two independently successful search channels (PubMed, Crossref) and a dedicated iodine reference source, not solely a tooling artifact.

Oxidative Stress

Each finding below is counted once, in this area only.

Oxidative stress, mixed, direction-dependent evidence

Yellow โ€” Low

See study details

Two separate, non-drug-specific literatures point in different directions. In selenium-deficient thyroid tissue, the H2O2 generated to organify iodide becomes damaging rather than merely consumed (Tier B rat model). Separately, an older theoretical paper proposes iodide itself as a primitive extrathyroidal antioxidant (Tier C narrative). Neither directly studies potassium iodide as a therapeutic agent.

Full detail, limits and 2 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. YELLOW

Limits on what this shows

  • Key null/negative: None identified specific to potassium iodide dosing; no human oxidative-stress biomarker study of SSKI or ThyroShield administration was located despite Crossref searches across multiple phrasings.

Population evidence

Contempre B et al., Endocrinology 2004;145(2):994-1002 (PMID 14500569). Rat model, selenium- and/or iodine-deficient thyroids with thiocyanate overload. Necrotic thyrocytes rose from 5.5% ยฑ 0.3% (iodine-deficient, selenium-replete) to 18.9% ยฑ 1.6% (iodine- and selenium-deficient plus thiocyanate-overloaded), a roughly 3.5-fold increase; selenium-deficient thyroids specifically progressed to fibrosis, selenium-replete ones did not. Authors propose combined iodine/selenium deficiency raises H2O2 accumulation while selenium deficiency separately impairs the glutathione-peroxidase-mediated cellular defense against that H2O2. Methimazole (which blocks organification and thus H2O2 generation) prevented the necrosis, mechanistically implicating the organification step itself.

Mechanism

Thyroid peroxidase uses H2O2 as a cosubstrate to organify iodide onto thyroglobulin; selenium-dependent glutathione peroxidase ordinarily limits collateral H2O2 damage. This is a mechanism of iodine-organification chemistry generally, not a potassium-iodide-drug-specific toxicity pathway, and the cited model used iodine deficiency plus thiocyanate, not exogenous potassium iodide dosing.

Tier and bound

Tier B, animal only, and not a study of potassium iodide administration. A second, separate line (Venturi S. Eur J Endocrinol 1999;140(4):371-372, PMID 10097259, "Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant?") is a 2-page theoretical/narrative commentary, Tier C, proposing iodide as an ancient antioxidant in thyroid and gastric mucosa; full abstract text was gated behind a publisher paywall this session and only the article's type, PMID and page range could be confirmed, disclosed here rather than the content being over-claimed.

Overlap

Shares its underlying source (Contempre et al. 2004) with the Selenium entry below, see Overlap map.

Counter-evidence held on record

Mechanistic and theoretical only, drawn from iodine-deficiency and narrative-review literature rather than potassium-iodide-drug data. Not evidence that potassium iodide itself raises or lowers human oxidative stress, and not a rationale for any antioxidant supplement.

Copper and Iron Balance

Copper and iron are assessed separately. Nothing here is counted twice.

Iron, reverse-direction interaction

Yellow โ€” Low

See study details

In iodine-deficient, goitrous children, iron-deficiency anemia measurably reduced the thyroid's response to iodine repletion therapy (iodized oil or iodized salt), and correcting the iron deficiency improved that response. This documents iron status affecting the response to iodine therapy, the reverse of potassium iodide depleting iron, and is drawn from iodine-repletion-of-deficiency studies rather than potassium-iodide-specific data.

Full detail and limits

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. YELLOW

Limits on what this shows

  • Key null/negative: None identified specific to potassium iodide; no study measuring iron status before/after SSKI or ThyroShield dosing was located.

Population evidence

Zimmermann M, Adou P, Torresani T, Zeder C, Hurrell R. "Iron supplementation in goitrous, iron-deficient children improves their response to oral iodized oil." Eur J Endocrinol 2000;142(3):217-223 (accessed via Crossref API metadata/abstract snippet: "iron supplementation may improve the efficacy of oral iodized oil in goitrous children with iron-deficiency anemia"). Zimmermann MB, Zeder C, Chaouki N, Torresani T, Saad A, Hurrell RF. "Addition of microencapsulated iron to iodized salt improves the efficacy of iodine in goitrous, iron-deficient children." Eur J Endocrinol 2002;147(6):747-753 (same access method; abstract snippet: "addition of encapsulated Fe to iodized salt improves the efficacy of iodine in goitrous children with a high prevalence of anemia"). A third, related trial (Hess SY, Zimmermann MB, Adou P, Torresani T, Hurrell RF. Am J Clin Nutr 2002;75(4):743-748) was located by title/journal/DOI via Crossref but not independently opened this session; listed in Sources for disclosure, not used as tier-defining evidence.

Mechanism

Thyroid peroxidase is a heme-dependent enzyme; iron deficiency is proposed to reduce thyroid peroxidase activity and thus blunt the thyroid's ability to use newly available iodine to synthesize hormone, independent of iodine supply itself.

Tier and direction

Tier A for the two independently accessed human RCTs, both from the same iodine-deficiency-correction research program (Zimmermann and colleagues, West African cohorts) rather than fully independent research groups, noted here as a boundary rather than presented as broader corroboration. The studied intervention in all three trials is iron and/or iodized oil/salt in iron- and iodine-deficient children, not potassium iodide (SSKI/ThyroShield) administration; per Hard Rule 4, this is filed as a direction-reversed context flag, not a depletion claim against potassium iodide.

Counter-evidence held on record

This describes iron status affecting response to iodine therapy in populations with endemic iodine deficiency, not potassium iodide depleting iron, and carries no supplement-dosing implication for patients receiving potassium iodide for thyroid storm or radiation blocking. If a patient's response to iodine-based thyroid therapy is unexpectedly poor, iron status is a documented (though indirect) factor worth a clinician's consideration, not a self-directed supplement decision.

Copper

Not graded โ€” disclosed evidence gap

See study details

No evidence at any tier connects potassium iodide to copper or ceruloplasmin status, and no circulating consumer claim exists to rebut.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. UNGRADED

Limits on what this shows

  • Why no grade: Both conditions for UNGRADED are met: (1) no Tier B or Tier C evidence links potassium iodide, or the iodide/iodine class generally, to copper or ceruloplasmin status; (2) no circulating consumer nutrient-depletion claim naming potassium iodide and copper was found in the sources checked (US Pharmacist and chiro.org drug-nutrient-depletion compilations were both opened and searched; neither mentions potassium iodide, iodine, or any thyroid drug at all, see Sources).

Search channels tried, this revision (2026-09-28)

This category was genuinely re-searched, not carried forward. A Crossref API query ("potassium iodide copper ceruloplasmin") loaded successfully and returned six works, all copper-iodide inorganic chemistry or copper-protein biochemistry papers unrelated to iodine's biological effect on copper status. A second Crossref query ("iodine trace element interaction copper zinc selenium") also loaded and surfaced one directly relevant epidemiological null: Duyar & Dedebayraktar 1999, Biol Trace Elem Res, reported that iodine and zinc, but not selenium or copper, deficiency was present in a male Turkish population with endemic goiter, a Tier C finding for a different drug context (endemic deficiency, not potassium iodide) that positively argues against a copper association rather than merely failing to find one (title/journal/year confirmed via Crossref metadata; full text not independently opened this session). A follow-up "potassium iodide" plus copper query was refused this session with an explicit do-not-retry HTTP 429 from the fetch proxy; PubMed and Europe PMC copper-specific queries were likewise refused. This is now a confirmed absence of supportive Tier B/C evidence, reinforced by one located null/counter finding, across a genuinely successful search channel, not solely a tooling artifact.

Gut Microbiome Risk

Each finding below is counted once, in this area only.

Gut microbiome risk, class-level evidence only

Yellow โ€” Low

See study details

A mouse study using sodium iodate, a different inorganic iodine-delivering salt than potassium iodide, found that ten weeks of supplemental iodine-compound intake measurably increased gut microbiota diversity and shifted its taxonomic composition, with the pattern diverging sharply by sex and several female-enriched taxa trending toward a more pro-inflammatory profile. This is class-level evidence for an iodine-compound load affecting the gut microbiome, not a potassium-iodide-specific or human finding.

Full detail, limits and 2 references

What the grade means here: Mechanistic plausibility only (Tier B), or class extrapolation (Tier C) with no drug-specific human status data; also used for context flags and interactions running the other direction. YELLOW

Limits on what this shows

  • Key null/negative: The Firmicutes and Proteobacteria increases were not statistically significant (P>0.05) despite trending upward; only the Bacteroidetes decrease and the two diversity indices reached significance. No human study, and no study of potassium iodide, SSKI, or ThyroShield specifically, connecting the drug to the gut microbiome was located in this or the original review session.

Population evidence

Shen H, Xu J, Lu C, Han J, Zhou J, Ming T, Li Y, Su X. "Effects of the Sex Factor on Mouse Iodine Intake: Interactions between the Gut Microbiota Composition and Metabolic Syndromes." ACS Omega 2021;6(43):28569-28578 (PMCID PMC8567277). ICR mice, four groups of n=6 (female saline control, male saline control, female sodium-iodate-supplemented, male sodium-iodate-supplemented); 18 ฮผg/kg/day sodium iodate by oral gavage for 10 weeks on top of standard iodine-sufficient chow, fecal 16S rRNA sequencing at weeks 0, 3, 6, 9. Shannon and Chao1 diversity indices rose significantly in both sexes in the iodine-supplemented group versus saline controls (P<0.05), with a larger shift in males. At the phylum level, Bacteroidetes decreased significantly (P<0.05) while Firmicutes and Proteobacteria trended higher without reaching significance (P>0.05). Taxon-level shifts were sex-divergent: females gained Desulfovibrionaceae, Enterococcus, and Clostridium, taxa the authors characterize as potentially pathogenic or pro-inflammatory, while males gained Faecalibacterium prausnitzii, Lactobacillus, and Bifidobacterium, taxa generally regarded as anti-inflammatory or probiotic.

Mechanism

Not fully elucidated in the source; the authors propose that supplemental iodine-compound intake reshapes gut microbial community structure differently by sex, and speculate this sex-divergent shift may partly explain the higher prevalence of clinical thyroid dysfunction in women. No mechanism specific to potassium iodide's much higher, acute or short-course thyroid-blocking doses is described or tested.

Tier and bound

Tier C for potassium iodide specifically: the studied compound was sodium iodate (NaIO3), a different inorganic iodine salt, in mice, at a comparatively low supplemental dose (18 ฮผg/kg/day) rather than the multi-hundred-milligram oral potassium iodide doses used in thyroid storm or radiation-blocking therapy. Graded yellow as class-level extrapolation per protocol: a real, opened, class-member study shows an iodine-compound-driven gut-microbiota effect, and the mechanism, an iodine-delivering inorganic salt reaching the gut, is plausible for potassium iodide, but this is not confirmed drug-specific or human evidence and the dose relationship to clinical KI regimens is unknown.

Access note

The publisher's own page (pubs.acs.org, via the DOI resolver) again returned an explicit do-not-retry HTTP 429 response this session, consistent with the original review's finding. This revision located and opened the article in full via its legitimate open-access repository mirror on PubMed Central (PMCID PMC8567277, author-submitted-version manuscript; open-access "gold" status and the repository listing were separately confirmed via the Unpaywall API), resolving the prior session's disclosed tooling-limited near-miss.

Counter-evidence held on record

This is class-level mouse evidence for a different iodine salt (sodium iodate), not a human or potassium-iodide-specific finding, and must not be read as evidence that potassium iodide disrupts the human gut microbiome. No probiotic, prebiotic, or microbiome-support supplement is recommended on the basis of this entry.

Oxygen and ATP Output

Oxygen delivery and ATP production are assessed separately. Nothing here is counted twice.

Oxygen delivery/utilization

Not graded โ€” disclosed evidence gap

See study details

No drug-specific or class-level evidence connects potassium iodide to hemoglobin, hematocrit, red-cell mass or tissue oxygen delivery, and no circulating consumer claim to rebut was found.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. UNGRADED

Limits on what this shows

  • Why no grade: Both UNGRADED conditions are met: (1) no Tier B/C evidence links potassium iodide to hemoglobin or oxygen-carrying capacity as a direct drug effect; (2) no circulating consumer claim naming potassium iodide and anemia, hemoglobin or "oxygen delivery" was found. Thyroid hormone status broadly affects erythropoiesis and metabolic oxygen demand in general endocrinology, but per Hard Rule 2 that pathway runs through the drug's intended pharmacologic target (suppressing thyroid hormone release in thyroid storm), not a direct nutrient-style effect of potassium iodide on oxygen delivery, and is excluded here rather than filed as a finding.

Search channels tried, this revision (2026-09-28)

This category was genuinely re-searched, not carried forward. Two Crossref API queries loaded successfully ("iodine induced hypothyroidism erythropoietin hemoglobin anemia"; "iodine deficiency anemia hemoglobin goiter") and together returned 16 works: two 1963 Lancet papers on iodine-induced hypothyroidism, a reticulocyte-hemoglobin-equivalent/iron-deficiency study in hypothyroid patients, and several unrelated erythropoietin/chemotherapy-anemia papers; none examined potassium iodide's or iodide's direct effect on hemoglobin, hematocrit, or oxygen-carrying capacity. The NIH Office of Dietary Supplements iodine health-professional fact sheet was opened and searched in full; it contains no mention of hemoglobin, anemia, or oxygen delivery. A PubMed query on the same terms and a further "potassium iodide" plus hemoglobin/hematocrit Crossref query were both refused this session with an explicit do-not-retry HTTP 429 from the fetch proxy; Europe PMC, OpenAlex, and Semantic Scholar queries were also refused (429) and not force-retried per instruction. This is now a confirmed absence of Tier B/C evidence across a genuinely successful search channel and a dedicated iodine reference source, not solely a tooling artifact.

ATP production

Not graded โ€” disclosed evidence gap

See study details

No drug-specific or class-level evidence connects potassium iodide directly to mitochondrial ATP synthesis or cellular energy output, and no circulating consumer claim to rebut was found.

Full detail and limits

What the grade means here: Nothing has been measured here, so this finding cannot be graded. That does not establish either safety or harm, and it is not the same as a White result. UNGRADED

Limits on what this shows

  • Why no grade: Both UNGRADED conditions are met: (1) no Tier B/C evidence links potassium iodide, or iodide/iodine generally, to ATP synthesis or cellular energy output as a direct drug effect; (2) no circulating consumer claim naming potassium iodide and "low energy"/ATP was found in the sources checked. As with Mitochondrial burden and Oxygen delivery/utilization, thyroid hormone's well-established general role in cellular energy metabolism is excluded here under Hard Rule 2 because it runs through the drug's intended pharmacologic target (thyroid hormone suppression) rather than constituting a direct nutrient-style ATP-production effect of the drug itself.

Search channels tried, this revision (2026-09-28)

This category was genuinely re-searched, not carried forward. A Crossref API query ("potassium iodide ATP cellular energy metabolism") was refused (HTTP 429); a follow-up, differently phrased query ("iodide thyrocyte ATP synthesis oxidative phosphorylation") loaded successfully and returned four general oxidative-phosphorylation reference works (an EcoSal chapter, two textbook chapters, one duplicate), none mentioning iodide or potassium iodide. The Mitochondrial burden entry's PubMed and Crossref searches, which used overlapping ATP/respiration terms, are cross-referenced here and likewise surfaced nothing iodide-specific. The NIH Office of Dietary Supplements iodine health-professional fact sheet was opened and searched in full; it contains no mention of ATP or cellular energy production. Europe PMC and Semantic Scholar queries were refused (429) this session and not force-retried per instruction. This is now a confirmed absence of Tier B/C evidence across two genuinely successful search channels (PubMed via the Mitochondrial burden entry, Crossref) and a dedicated iodine reference source, not solely a tooling artifact.

Claims checked and not supported

These circulate online for this medication. They are listed here only so they can be answered, never as findings, and they are not graded.

A claim with no supporting evidence is not necessarily disproven. Where evidence actually argues against a claim, that is stated below.

  • High-dose iodine / potassium iodide "flushes out" toxic halides (bromide, fluoride, chlorine) from the body, and urinary bromide excretion after an iodine "loading test" proves this detoxification

    Where it comes from: General claim circulating in high-dose-iodine supplementation communities (the "iodine loading test" / halide-displacement protocol associated with popular iodine-advocacy sources). Not found in the two standard drug-nutrient-depletion compilations checked (US Pharmacist; chiro.org), which do not mention potassium iodide or iodine at all.

    Why it fails: The one drug-adjacent primary source located this session, Waugh 2019 ( Int J Environ Res Public Health 16(6):1086), describes fluoride inhibiting sodium-iodide symporter expression and function, impairing iodide absorption, the opposite mechanism direction from iodide actively displacing or excreting stored fluoride from the body. No clinical study measuring a meaningful reduction in whole-body bromide or fluoride burden from potassium iodide dosing was found despite search (accessed via Crossref API metadata/abstract field; the full publisher page was not independently opened this session due to proxy rate-limiting, disclosed in Sources). Elevated urinary halide excretion after a large iodide dose is consistent with simple renal competition for excretion at the time of dosing, not with a documented reduction in total-body halide stores.

All references used above
  1. SSKI (potassium iodide) oral solution, full prescribing information. โ€” DailyMed, National Library of Medicine, packager Avondale Pharmaceuticals LLC. Opened in full; source for pharmacokinetic basis, mechanism, hypothyroidism warning, hyperkalemia/potassium-sparing-agent interaction, iodism symptoms, dosing, pregnancy/lactation warnings, and the DESI/unapproved-labeling regulatory-status note. Notes: labeled indication is as an expectorant; this label does not itself describe thyroid-storm use.
  2. ThyroShield (potassium iodide) oral solution, full prescribing information. โ€” DailyMed, National Library of Medicine, packager Fleming & Company, Pharmaceuticals. Opened in full; source for the radiation thyroid-blocking mechanism, dosing table by age/weight, contraindications (dermatitis herpetiformis, hypocomplementemic vasculitis, nodular thyroid disease with cardiac disease), adverse reactions, and neonatal/pregnancy monitoring guidance.
  3. Potassium iodide. โ€” Wikipedia. Opened; used only as a tertiary cross-check for ATC code listings (R05CA02, S01XA04, V03AB21) and general orientation. The primary WHO ATC/DDD Index (atcddd.fhi.no) was directly attempted this session but blocked by the tooling proxy (HTTP 429, explicit do-not-retry response); the ATC codes reported in this dossier are therefore sourced from this tertiary reference and disclosed as not independently confirmed against the WHO primary source this session.
  4. Takano N, Seki Y, Watanabe D, Ichihara A. Drug-Induced Liver Injury Due to Potassium Iodide During Thyroid Storm. โ€” JCEM Case Reports 2026 (PMID 42022482). Single case report, 30-year-old male, Graves'-disease thyroid storm, KI 150 mg/day, peak total bilirubin 32.4 mg/dL on day 19, positive lymphocyte transformation test to KI (stimulation index 288%), rapid resolution after KI discontinuation. Opened in full via academic.oup.com; source for the monitoring-panel liver-injury disclosure. Not graded as a nutrient-category entry (hepatic injury falls outside this dossier's nutrient/physiological-category scope).
  5. Contempre B, Morreale de Escobar G, Denef JF, Dumont JE, Many MC. Thiocyanate Induces Cell Necrosis and Fibrosis in Selenium- and Iodine-Deficient Rat Thyroids. โ€” Endocrinology 2004;145(2):994-1002 (PMID 14500569). Rat model, Tier B. Opened via academic.oup.com (abstract-level detail); source for the Oxidative stress and Selenium entries, and for the Overlap map row linking them.
  6. Contempre B, Dumont JE, Ngo B, Thilly CH, Diplock AT, Vanderpas J. Effect of selenium supplementation in hypothyroid subjects of an iodine and selenium deficient area: the possible danger of indiscriminate supplementation of iodine-deficient subjects with selenium. โ€” J Clin Endocrinol Metab 1991;73(1):213-215 (PMID 2045471). Human supplementation study, northern Zaire, Tier A. Opened via academic.oup.com (abstract-level detail); source for the Selenium entry.
  7. Venturi S, Venturi M. Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant? โ€” Eur J Endocrinol 1999;140(4):371-372 (PMID 10097259). Narrative/theoretical commentary, Tier C. Opened via academic.oup.com; only the article type, PMID, and page range (a 2-page commentary) were accessible, the full abstract text was gated behind a publisher paywall this session. Used in the Oxidative stress entry only as a disclosed, limited-access theoretical source, not as a tier-raising data source.Full abstract text gated by publisher paywall; only metadata (PMID, article type, pages) was accessible this session.
  8. Zimmermann M, Adou P, Torresani T, Zeder C, Hurrell R. Iron supplementation in goitrous, iron-deficient children improves their response to oral iodized oil. โ€” Eur J Endocrinol 2000;142(3):217-223. Human RCT, Tier A. Accessed via Crossref API metadata including an abstract-derived key-finding snippet; the full publisher page was not independently opened this session. Source for the Iron entry.Accessed via Crossref API abstract snippet only; full publisher page not independently opened this session.
  9. Zimmermann MB, Zeder C, Chaouki N, Torresani T, Saad A, Hurrell RF. Addition of microencapsulated iron to iodized salt improves the efficacy of iodine in goitrous, iron-deficient children. โ€” Eur J Endocrinol 2002;147(6):747-753. Human RCT, Tier A. Accessed via Crossref API metadata including an abstract-derived key-finding snippet; the full publisher page was not independently opened this session. Source for the Iron entry.Accessed via Crossref API abstract snippet only; full publisher page not independently opened this session.
  10. Hess SY, Zimmermann MB, Adou P, Torresani T, Hurrell RF. Treatment of iron deficiency in goitrous children improves the efficacy of iodized salt in Cote d'Ivoire. โ€” Am J Clin Nutr 2002;75(4):743-748. Human RCT, Tier A by title/journal. Located via Crossref API (title, authors, journal, DOI only); not independently opened or read this session. Listed for disclosure; not used as tier-defining evidence in the Iron entry.Located via Crossref metadata only; not independently opened this session.
  11. Waugh DT. Fluoride Exposure Induces Inhibition of Sodium/Iodide Symporter (NIS) Contributing to Impaired Iodine Absorption. โ€” Int J Environ Res Public Health 2019;16(6):1086. Narrative review, Tier C, not potassium-iodide-specific. Accessed via Crossref API metadata/abstract field; the full publisher page (pubs.acs.org-equivalent MDPI site) returned HTTP 429 when directly fetched and was not independently opened this session. Source for the halide-detoxification Fails-verification entry.Full publisher page blocked (HTTP 429) this session; accessed via Crossref API abstract-field metadata only.
  12. Drug-Induced Nutrient Depletions: What Pharmacists Need to Know. โ€” US Pharmacist (consumer/professional circulating-claims source). Opened and searched for potassium iodide, iodine, SSKI, Lugol's solution, thyroid drugs, methimazole, propylthiouracil; no matches found. Used as negative evidence in the circulating-claim audit.
  13. Drug-Nutrient Depletion and Interaction Charts. โ€” Chiro.org compilation (consumer/practitioner circulating-claims source). Opened and searched for potassium iodide, iodine, SSKI, Lugol's solution, thyroid drugs, and selenium/thyroid content; no relevant matches found. Used as negative evidence in the circulating-claim audit.
  14. Kusunoki M, Fujihara T, Ishida R, Yamamori Y. Hyperkalemia Caused by Potassium-Enriched Salt in a Hospitalized Patient. โ€” Cureus 2025 (DOI 10.7759/cureus.86704). Single case report, Tier C for this drug (potassium-enriched table salt, not potassium iodide). Located and summarized via Crossref API; used only as class-level plausibility context in the Potassium entry, not counted toward that entry's tier.
  15. Yeung SJ, Go R, Balasubramanyam A. Rectal Administration of Iodide and Propylthiouracil in the Treatment of Thyroid Storm. โ€” Thyroid 1995;5(5):403-405. Located via Crossref API (title, authors, journal, DOI only); not independently opened this session. Listed for disclosure and as context on drug-specific clinical use in thyroid storm, not used as tier-defining evidence.Located via Crossref metadata only; not independently opened this session.
  16. Becker DV, Zanzonico P. Potassium Iodide for Thyroid Blockade in a Reactor Accident. โ€” Thyroid 1997;7(2):193-194. Located via Crossref API (title, authors, journal, DOI only); not independently opened this session. Listed for disclosure and as context on radiation thyroid-blocking use, not used as tier-defining evidence.Located via Crossref metadata only; not independently opened this session.
  17. Ahmadi S. The Use of Potassium Iodide in Patients with Thyroid Storm. โ€” Clinical Thyroidologyยฎ 2024;36:172-174. Located via Crossref API (title, authors, journal, DOI only); not independently opened this session. Listed for disclosure only, not used as tier-defining evidence.Located via Crossref metadata only; not independently opened this session.
  18. Shen H, Xu J, Lu C, Han J, Zhou J, Ming T, Li Y, Su X. Effects of the Sex Factor on Mouse Iodine Intake: Interactions between the Gut Microbiota Composition and Metabolic Syndromes. โ€” ACS Omega 2021;6(43):28569-28578 (DOI 10.1021/acsomega.1c02697; PMCID PMC8567277). Mouse study (ICR mice, n=6/group, sodium iodate 18 ฮผg/kg/day by gavage x10 weeks, fecal 16S sequencing), Tier C source for Gut microbiome risk (different iodine compound than potassium iodide). Opened and read in full this revision (2026-09-28) via its open-access repository mirror on PubMed Central after the publisher page again refused access; source for the Gut microbiome risk entry's diversity indices, phylum-level and taxon-level findings, and study design.
  19. Unpaywall API (api.unpaywall.org), query by DOI 10.1021/acsomega.1c02697. โ€” Opened successfully this revision (2026-09-28); returned the open-access status and repository location list (Europe PMC, PubMed Central, DOAJ) for the Shen et al. 2021 ACS Omega article above, which led directly to the PubMed Central mirror used to open it.
  20. Office of Dietary Supplements, National Institutes of Health. Iodine, Health Professional Fact Sheet. โ€” Opened and read in full this revision (2026-09-28); searched specifically for mitochondria, copper/ceruloplasmin, gut microbiome, hemoglobin/anemia/oxygen delivery, and ATP/cellular energy content. None found. Used as confirmatory negative evidence in the Mitochondrial burden, Copper, Oxygen delivery/utilization, and ATP production ungraded entries.
  21. Duyar I, Dedebayraktar D. Iodine and zinc, but not selenium and copper, deficiency exists in a male Turkish population with endemic goiter. โ€” Biol Trace Elem Res 1999. Located via Crossref API this revision (2026-09-28) (title, journal, year confirmed; full text not independently opened this session). Tier C for potassium iodide (endemic-deficiency population, not a drug-exposure study); a positive null finding, no copper-deficiency association found alongside confirmed iodine deficiency. Cited in the Copper ungraded entry as counter-evidence reinforcing the gap, not as tier-raising support.Located via Crossref metadata only; full text not independently opened this session.
  22. PubMed search-listing pages (pubmed.ncbi.nlm.nih.gov), multiple query phrasings. โ€” Original session: attempted for potassium iodide plus thyroid storm, hyperkalemia, and oxidative stress terms, all rejected (HTTP 429, explicit do-not-retry). This revision (2026-09-28): a "potassium iodide mitochondria" query loaded successfully and 10 results were opened and read in full (see Mitochondrial burden entry); a follow-up hemoglobin/anemia query and a repeat copper query were then rejected again (HTTP 429, explicit do-not-retry). Access is intermittent rather than uniformly blocked; results are used as evidence only where a fetch actually succeeded and returned content, per entry.Intermittent: one query succeeded and was read in full this revision; further queries were refused (HTTP 429, explicit do-not-retry) and not force-retried.
  23. Europe PMC REST API and website (www.ebi.ac.uk). โ€” Attempted again this revision (2026-09-28) via two fresh queries (hemoglobin/oxygen; ATP/mitochondria terms), both rejected by the fetch proxy with an explicit do-not-retry HTTP 429, consistent with the original session's finding. A direct command-line check of the underlying network policy this revision showed www.ebi.ac.uk is denied at the organization's egress-policy level (HTTP 403 on the CONNECT tunnel), independent of the WebFetch-tool-specific 429s, confirming this is a genuine, persistent access block rather than transient rate limiting. Not used as an evidence source.Blocked both at the WebFetch-tool layer (do-not-retry HTTP 429) and, independently confirmed this revision, at the organization egress-policy layer (HTTP 403).
  24. OpenAlex API (api.openalex.org) and Semantic Scholar API (api.semanticscholar.org). โ€” Attempted again this revision (2026-09-28) for oxygen-delivery, ATP/mitochondria, and hemoglobin terms; both returned persistent HTTP 429 directly from the target servers (Semantic Scholar) or from the organization's egress policy (OpenAlex, confirmed HTTP 403 on the CONNECT tunnel via a direct command-line check). Not used as an evidence source this revision.OpenAlex blocked at the organization egress-policy level (HTTP 403); Semantic Scholar returned persistent HTTP 429 from the target server.
  25. Crossref API (api.crossref.org), multiple query phrasings across all five categories re-examined this revision. โ€” This revision (2026-09-28): loaded successfully for Gut microbiome risk (led to the Unpaywall/PMC chain above), Mitochondrial burden (2 queries), Copper (2 queries, including the Duyar & Dedebayraktar 1999 null finding), Oxygen delivery/utilization (2 queries), and ATP production (1 of 2 queries; the other returned HTTP 429). Crossref was the single most reliable channel this revision and supplied the bulk of the fresh evidence and null results cited in the updated entries above.Mostly successful this revision; one ATP-production query returned HTTP 429 and was not force-retried, a differently phrased follow-up succeeded.
  26. WebSearch tool. โ€” Original session: four queries attempted, all returned "session has used its web search budget (200 of 200 WebSearch calls)" before results were produced. This revision (2026-09-28): a fresh query for the ACS Omega/gut-microbiome candidate was attempted first and returned the identical exhausted-budget message, confirming the budget is account-level and shared across sessions in this dossier batch, not session-specific; not re-attempted further given that confirmation.Session/account-level WebSearch budget exhausted (200/200) on every attempt across both the original session and this revision.
  27. WHO Collaborating Centre for Drug Statistics Methodology, ATC/DDD Index (atcddd.fhi.no). โ€” Attempted directly for ATC code H03CA01/R05CA02 verification. Blocked by the tooling proxy (HTTP 429, explicit do-not-retry response). Not independently confirmed this session; ATC codes in this dossier are sourced from Wikipedia's tertiary listing instead, disclosed above. Not re-attempted this revision, as this fact was not part of the five re-researched categories.Blocked by the tooling proxy (HTTP 429, explicit do-not-retry response).
  28. Bing web search and DuckDuckGo HTML search. โ€” Attempted as an alternative to the blocked WebSearch tool and literature APIs, both original session and this revision. Bing returned "URL is disallowed by robots.txt rules" both times; DuckDuckGo's HTML endpoint returned a robots.txt fetch timeout. Neither was usable.Both blocked by robots.txt/connection failure on every attempt.