Iodine excess.
Level 5 - mechanism / opinion, no new human data
Narrative review and mechanism-based reasoning without systematic methodology
PubMed 20172475 · doi:10.1016/j.beem.2009.08.010
What was done
This is a narrative review summarizing the physiological mechanisms that regulate thyroid hormone synthesis during iodine excess and the pathophysiological pathways leading to iodine-induced thyroid dysfunction.
What was found
The abstract details that the thyroid maintains normal hormone secretion even when iodine intake exceeds physiologic needs by 100-fold. Acute excess acutely blocks iodide organification (Wolff-Chaikoff effect) at intracellular iodide concentrations ≥10^-3 M. This block is transient because the sodium-iodide symporter downregulates, reducing intracellular iodide below 10^-3 M. In susceptible individuals (e.g., following radio-iodine therapy or with autoimmune thyroiditis), failure of this escape leads to chronic hypothyroidism. In individuals with autonomous nodules (such as from prior iodine deficiency), excess iodine can cause hyperthyroidism. The abstract reports mechanistic concentrations but provides no clinical cohort numerical data.
Why it matters
This paper outlines the mechanistic basis for how excess iodine can trigger opposite clinical outcomes—hypothyroidism or hyperthyroidism—depending on underlying thyroid susceptibility and historical iodine exposure.
Limits
As a narrative review, there is no systematic literature search, risk-of-bias assessment, or pooled clinical data. Precise incidence rates, human risk estimates, and exposure thresholds in clinical populations are not reported.
Cited by
- supports Excessive intake of iodine temporarily shuts down or pauses biochemical reactions in the thyroid gland.