tuneTypical Dose
150-300 mcg per day
Mineral
Iodine
Iodine (I, element 53)
Evidence TierAWADA NOT PROHIBITED
watchEffect Window
Weeks for biochemical normalization of thyroid markers in deficiency correction.
check_circleCompliance
WADA NOT PROHIBITED
Overview
Clinical Summary
Iodine is required for thyroid hormone synthesis and normal growth and neurodevelopment. It is used to correct low iodine intake, particularly in pregnancy and in low seafood or iodized salt diets.
Correcting iodine deficiency prevents goiter and hypothyroid symptoms and supports fetal and infant neurodevelopment. Benefits are clearest in populations with low baseline intake. Minority evidence suggests improvement in fibrocystic breast discomfort in some individuals. Excess iodine can precipitate thyroid dysfunction, especially in autoimmune thyroid disease, so benefit depends on restoring adequacy rather than high dosing.
Essential substrate for thyroid peroxidase-mediated synthesis of T4 and T3. Iodide is actively transported into thyroid follicular cells via the sodium-iodide symporter, organified, and coupled to form thyroid hormones.
Outcomes
What This Is Expected To Influence
Primary Outcomes
- Prevents goiter and cretinism in iodine-deficient populations
- Normalizes thyroid hormone levels (T3, T4, TSH) in deficiency
Secondary Outcomes
- Supports cognitive development in iodine-deficient children
- Maintains adequate urinary iodine concentration
Safety
Contraindications and Interactions
Contraindications
- Hashimoto's thyroiditis (may worsen)
- Graves' disease
- Uncontrolled thyroid disease
Side effects
- Metallic taste
- GI upset (nausea, stomach pain)
- Acne-like skin lesions at high doses
Interactions
- Amiodarone (additive thyroid suppression)
- Lithium (additive thyroid suppression)
- Anti-thyroid medications (antagonism)
Avoid if
- Autoimmune thyroid disease without medical supervision
- Iodine hypersensitivity
Evidence
Study-level References
iodine-SRC-001Narrative review of human epidemiology and intervention evidence.
Sourceopen_in_newZimmermann MB. Iodine deficiency. Endocr Rev. 2009;30(4):376-408.
Population: General populations with emphasis on iodine-deficient regions, pregnancy, and child neurodevelopment outcomes.
Dose protocol: Population iodine prophylaxis/supplementation strategies. Adequacy framed around physiological intake targets.
Key findings: Iodine deficiency is a leading preventable cause of thyroid dysfunction and impaired neurodevelopment worldwide. Adequate iodine intake prevents endemic goiter and iodine-deficiency hypothyroidism. Maternal iodine deficiency is linked to adverse fetal brain outcomes. Prevention is a core public-health priority. Excess iodine exposure can induce thyroid dysfunction in susceptible individuals, supporting dose-range discipline.
Notes: Workbook context flags non-iodized salt adoption as a practical driver of deficiency re-emergence in some cohorts.
Paper content
Iodine deficiency is a leading preventable cause of thyroid dysfunction and impaired neurodevelopment worldwide. Adequate iodine intake prevents endemic goiter and iodine-deficiency hypothyroidism. Maternal iodine deficiency is linked to adverse fetal brain outcomes; prevention is a core public-health priority. Excess iodine exposure can induce thyroid dysfunction in susceptible individuals, supporting dose-range discipline.