Iodine: Understanding Your Blood Test Series

1. Overview: What this test reveals and why it is important

Iodine is an essential trace element and a critical component of the thyroid hormones thyroxine (T4) and triiodothyronine (T3). These hormones regulate virtually every aspect of human metabolism, including basal metabolic rate, protein synthesis, enzyme activity, and neurological development. The human body contains approximately 15–20 mg of iodine, more than 70% of which is concentrated in the thyroid gland.

Iodine status is assessed because both deficiency and excess have profound health consequences:

· Iodine deficiency is the single most common cause of preventable intellectual disability worldwide. It affects an estimated two billion people globally, with pregnant women and young children being most vulnerable. Deficiency causes a spectrum of disorders collectively termed Iodine Deficiency Disorders (IDD), including goitre, hypothyroidism, cretinism, and impaired cognitive development.

· Iodine excess can also cause thyroid dysfunction, particularly in susceptible individuals – those with underlying autoimmune thyroid disease, the elderly, or those with previous iodine deficiency. Excess iodine can induce both hyperthyroidism (Jod‑Basedow phenomenon) and hypothyroidism (Wolff‑Chaikoff effect).

Measuring iodine status is challenging. Unlike many nutrients, iodine is not routinely measured in individual clinical practice due to technical difficulties and physiological variability. The preferred population‑level assessment is urinary iodine concentration (UIC), as more than 90% of dietary iodine is excreted in urine. In individual patients, clinicians typically assess thyroid function (TSH, FT4, FT3) and thyroid antibodies, with iodine testing reserved for specific indications:

· Suspected iodine deficiency in at‑risk populations

· Unexplained thyroid dysfunction

· Monitoring during iodine supplementation programmes

· Assessment before radioactive iodine therapy

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2. What does it measure

a. Units of measurement

· Urinary iodine concentration (UIC): Micrograms per litre (mcg/L)

· Serum iodine: Micrograms per litre (mcg/L) – less commonly used, reflects recent intake

· Thyroid iodine content: Measured by X‑ray fluorescence (research tool only)

b. Normal range and interpretation

Urinary iodine concentration (spot urine) – WHO epidemiological criteria for population assessment:

· Severe deficiency: <20 mcg/L

· Moderate deficiency: 20–49 mcg/L

· Mild deficiency: 50–99 mcg/L

· Adequate / optimal: 100–199 mcg/L

· More than adequate: 200–299 mcg/L

· Excessive: >300 mcg/L

For individual clinical interpretation, these cut‑offs are used cautiously. A single spot urine is highly variable day‑to‑day; 24‑hour urine collection or multiple spot samples provide more reliable individual data.

Serum iodine (reference ranges vary by laboratory):

· Typical reference interval: 40 – 80 mcg/L (0.32 – 0.63 µmol/L)

· Toxic levels: >200 mcg/L (associated with iodine‑induced hyperthyroidism)

Critical interpretive principle: Iodine status must be interpreted alongside thyroid function tests (TSH, FT4, FT3), thyroid antibodies (TPOAb, TgAb), and clinical context. A low UIC with normal thyroid function suggests adequate adaptation; a low UIC with elevated TSH indicates insufficient thyroid hormone synthesis.

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3. Other factors connected to this

a. Direct correlation (factors affecting iodine levels)

· Dietary intake: The primary determinant. Food iodine content varies dramatically by geography and agricultural practices.

· Geographical location and soil iodine content:

· Iodine‑replete regions: coastal areas, regions with iodised salt programmes, parts of North America, Scandinavia, Switzerland, Japan (high seafood and seaweed consumption)

· Iodine‑deficient regions: mountainous areas (Himalayas, Alps, Andes), flood‑prone river valleys, regions远离海洋 with glaciated soils – much of India (especially sub‑Himalayan belt), parts of Europe, Africa, Southeast Asia

· Iodised salt programmes: Universal salt iodisation is the most effective public health strategy. Coverage varies widely; non‑iodised salt (sea salt, pink Himalayan salt, rock salt) does not provide iodine.

· Pregnancy and lactation: Iodine requirements increase by approximately 50% due to increased thyroid hormone production, increased renal iodine clearance, and transfer to fetus/infant.

· Breastfeeding: Infants are entirely dependent on maternal milk iodine; maternal deficiency rapidly depletes infant stores.

b. Indirect correlation (factors influencing iodine requirements or thyroid function)

· Goitrogens: Substances that interfere with thyroid hormone synthesis or iodine uptake. Found in:

· Cruciferous vegetables (cabbage, cauliflower, broccoli, kale, radish, turnip) – contain thiocyanates and isothiocyanates

· Cassava, sweet potato, maize, lima beans – contain cyanogenic glycosides metabolised to thiocyanates

· Soy and soy products – isoflavones may inhibit thyroid peroxidase in susceptible individuals, especially with iodine deficiency

· Millet – contains C‑glycosylflavones

· Note: In iodine‑replete individuals, dietary goitrogens are clinically insignificant; cooking reduces their activity.

· Selenium status: Selenium is essential for thyroid hormone synthesis (deiodinases) and protects the thyroid from oxidative damage. Combined selenium and iodine deficiency worsens thyroid dysfunction.

· Iron deficiency: Impairs thyroid hormone synthesis; iron is a cofactor for thyroid peroxidase.

· Vitamin A deficiency: May exacerbate thyroid dysfunction in iodine deficiency.

· Autoimmune thyroid disease: Both Hashimoto's thyroiditis and Graves' disease alter iodine handling. Excess iodine can precipitate or worsen autoimmunity.

· Medications:

· Amiodarone – antiarrhythmic drug; contains 75 mg iodine per tablet (37% iodine by weight); causes thyroid dysfunction in up to 20% of users

· Radiocontrast agents – contain high iodine loads; can induce thyroid dysfunction

· Lithium – affects thyroid hormone release and may enhance goitrogenicity

· Sulfonylureas, phenytoin, carbamazepine – mild effects

· Renal function: Chronic kidney disease alters iodine excretion; interpretation complex.

· Age: Elderly individuals are more susceptible to iodine‑induced thyroid dysfunction.

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4. Disorders related to abnormal values

a. When low (iodine deficiency)

Iodine Deficiency Disorders (IDD) – spectrum from fetus to adult:

Fetal and neonatal:

· Abortion, stillbirth, congenital anomalies

· Cretinism: Two forms:

· Neurological cretinism: Severe intellectual disability, deaf‑mutism, spastic diplegia, strabismus – results from first‑trimester deficiency

· Myxoedematous cretinism: Profound hypothyroidism, growth retardation, developmental delay – results from combined iodine and selenium deficiency

· Neonatal hypothyroidism: Elevated TSH at birth

Child and adolescent:

· Goitre: Thyroid enlargement as compensatory response to low iodine

· Subclinical hypothyroidism: Elevated TSH, normal FT4

· Impaired cognitive development: Reduced IQ by 10–15 points in deficient populations

· Delayed physical development

Adult:

· Goitre: Can become nodular over time; may cause compressive symptoms

· Hypothyroidism: Fatigue, weight gain, cold intolerance, constipation, dry skin, bradycardia

· Impaired fertility

· Increased pregnancy complications: Miscarriage, preterm delivery

· Iodine deficiency during pregnancy: Offspring neurocognitive impairment

Causes of deficiency:

· Low dietary iodine (soil deficiency, no iodised salt, limited seafood/seaweed)

· Pregnancy and lactation without supplementation

· Vegan or plant‑based diets in low‑iodine regions without careful planning

· Exclusion of iodised salt (use of gourmet salts)

· Malabsorption (coeliac disease, Crohn's, cystic fibrosis)

· Chronic haemodialysis

b. When high (iodine excess)

Iodine‑induced thyroid dysfunction:

· Iodine‑induced hyperthyroidism (Jod‑Basedow phenomenon):

· Occurs in individuals with pre‑existing thyroid autonomy (nodular goitre, latent Graves' disease) or in previously iodine‑deficient populations after iodine supplementation

· Presents with weight loss, tachycardia, palpitations, anxiety, heat intolerance

· Iodine‑induced hypothyroidism:

· Failure to escape from the acute Wolff‑Chaikoff effect (transient inhibition of thyroid hormone synthesis by high iodine)

· Occurs in individuals with autoimmune thyroiditis (Hashimoto's), post‑partum thyroiditis, subacute thyroiditis, or after treatment with iodine‑containing drugs (amiodarone, radiocontrast)

· Presents with fatigue, weight gain, bradycardia, dry skin

Acute iodine toxicity (rare, massive ingestion):

· Burning mouth, throat, stomach

· Nausea, vomiting, diarrhoea

· Abdominal pain

· Shock, airway compromise (rare)

Chronic selenosis/siderosis (industrial exposure):

· Metallic taste, increased salivation

· Thyroid dysfunction as above

· Skin rashes, acneiform lesions

Causes of excess:

· Excessive iodine supplementation (dietary supplements containing iodine, kelp tablets)

· High dietary intake (Japan – seaweed consumption)

· Iodine‑containing medications (amiodarone, radiocontrast, topical iodine antiseptics)

· Occupational exposure

· Water contamination in certain regions

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5. Best way to address aberrant levels

Critical principle: Iodine requirements change across the lifespan, and the margin between deficiency and excess is narrower than for many nutrients. Intervention must be individualised, guided by laboratory assessment where possible, and always consider thyroid function. Never self‑prescribe iodine supplements without knowing your baseline status and without medical supervision, particularly if you have thyroid disease.

a. Quick ways or using Medications (Medical Management)

Iodine deficiency:

· Universal recommendation: Use iodised salt in cooking and at the table (unless contraindicated). This is the foundation of public health prevention.

· Iodised salt contains 15–40 mg iodine per kg salt; typical intake provides 150–300 mcg daily.

· Note: "Pink Himalayan salt," "sea salt," "rock salt," and "kosher salt" are NOT iodised unless specifically labelled. They do not correct deficiency.

· Oral iodine supplementation (for confirmed deficiency):

· Form: Potassium iodide (KI) or potassium iodate (KIO₃). Both are effective; iodate is more stable in humid tropical conditions.

· Dose:

· Adults (non‑pregnant): 150 mcg daily

· Pregnancy and lactation: 200–250 mcg daily

· Children (1–8 years): 90 mcg daily

· Children (9–13 years): 120 mcg daily

· Dosing forms: Single‑ingredient potassium iodide tablets (often 150 mcg or 225 mcg) are preferred. Avoid multi‑ingredient "thyroid support" blends with unknown iodine content.

· Monitoring: Recheck urinary iodine and thyroid function after 3–6 months.

· Treatment of goitre/hypothyroidism:

· Levothyroxine (T4): May be required if TSH is elevated, especially in pregnancy or if goitre causes compressive symptoms.

· Iodine supplementation alone: May be sufficient for simple iodine‑deficiency goitre with normal TSH, but resolution takes months.

· Pregnancy and lactation:

· All pregnant women in iodine‑deficient regions should receive a daily supplement containing 150 mcg iodine (as potassium iodide), ideally started pre‑conception.

· Prenatal vitamins: Many do NOT contain iodine; check labels carefully.

· Do not exceed 500 mcg daily in pregnancy; risk of fetal hypothyroidism.

Iodine excess / toxicity:

· Immediate withdrawal of all iodine‑containing supplements, medications (if possible), and high‑iodine foods.

· Management of thyroid dysfunction:

· Iodine‑induced hyperthyroidism: Beta‑blockers for symptoms; antithyroid drugs (methimazole, carbimazole) may be required. Refer to endocrinologist.

· Iodine‑induced hypothyroidism: Levothyroxine replacement if symptomatic or TSH persistently elevated. Condition may be transient; reassess after iodine withdrawal.

· Amiodarone‑induced thyroid dysfunction: Complex; requires specialist endocrinology input. Amiodarone cannot usually be stopped due to cardiac indications.

· Acute toxicity: Supportive care; no specific antidote. Activated charcoal if ingestion within 2 hours.

Do not self‑manage iodine excess. Seek medical attention immediately if toxicity is suspected, especially if taking amiodarone or after radiocontrast exposure.

b. Using Supplements or Holistic medicine

Iodine supplements (medical grade) are discussed above. The following are additional considerations and cautions.

· Kelp and seaweed supplements:

· Rationale: Seaweed is a natural, plant‑based source of iodine. However, iodine content is highly variable and unpredictable.

· Variability: Kelp (Ascophyllum nodosum, Laminaria spp.) can contain 50–3000 mcg iodine per gram. A single capsule may provide anywhere from 50 mcg to >1000 mcg.

· Risk: Easy to exceed safe upper limits (1100 mcg daily for adults) with regular consumption. Cases of iodine‑induced hyperthyroidism and hypothyroidism from kelp supplements are well documented.

· Recommendation: Not recommended as a reliable supplement for therapeutic dosing. If used, choose products that provide measured, standardised iodine content (mcg per serving) and do not exceed 150–200 mcg daily.

· Whole food sources (discussed in diet section).

· Herbs and Phytochemicals from Indian subcontinent:

Note: These herbs do NOT contain significant iodine. They may support thyroid function indirectly or modulate autoimmune activity, but they do not correct iodine deficiency.

· Guggulu (Commiphora mukul):

· Rationale: Gum resin used in Ayurveda for thyroid disorders ("kanthaka"). Contains guggulsterones, which may stimulate thyroid function in animal studies. Human evidence limited.

· Form: Standardised guggulsterone extract (2.5–5%).

· Caution: Do not use as a substitute for iodine or levothyroxine. May interact with other medications.

· Ashwagandha (Withania somnifera):

· Rationale: Adaptogen; some studies suggest it may increase T4 in subclinical hypothyroidism. Does not provide iodine.

· Form: Standardised root extract (withanolides 2.5–5%).

· Dose: 300–600 mg daily.

· Caution: Avoid in hyperthyroidism; may stimulate thyroid. Use only under guidance.

· Brahmi (Bacopa monnieri):

· Rationale: Cognitive enhancer; may support neurological function in iodine deficiency. No direct effect on thyroid.

· Form: Standardised extract (bacopasides).

· Tulsi (Ocimum sanctum):

· Rationale: Adaptogenic; may modulate stress response and support overall health.

· Form: Tea or leaf extract.

· Kanchanar (Bauhinia variegata):

· Rationale: Traditional Ayurvedic herb for goitre and lymph node disorders. Often combined with guggulu in formulations. Limited modern evidence.

· Important caution: Avoid proprietary "thyroid support" blends that combine iodine, tyrosine, guggulu, ashwagandha, and other herbs in unknown proportions. These are unregulated and may cause harm, especially in undiagnosed autoimmune thyroid disease.

· Synergistic nutrients:

· Selenium: Essential for thyroid hormone synthesis and antioxidant protection. Ensure adequate selenium status (see previous guide) before or alongside iodine supplementation in hypothyroidism, especially Hashimoto's.

· Iron: Iron deficiency impairs thyroid function; correct if present.

· Zinc and copper: Support thyroid health; ensure adequacy.

c. Using Diet and Foods (Following a plant‑forward, ecologically sustainable approach)

Dietary iodine intake is entirely dependent on soil and water iodine content, food choices, and the use of iodised salt. In low‑iodine regions, achieving adequate intake without iodised salt or supplements is extremely difficult. The ecological hierarchy guides choices, but adequacy must be ensured through fortified foods (iodised salt) or supplementation.

Plant‑based iodine sources (highly variable, often unreliable):

· Seaweed and sea vegetables: The only consistently rich plant‑based sources. However, content varies enormously by species, season, and harvest location.

Seaweed Type Typical Iodine Content (mcg/g dry weight)

Kelp (kombu) 1500 – 3000 (can exceed 8000)

Wakame 50 – 400

Nori (used for sushi) 10 – 50

Dulse 30 – 150

Arame, Hijiki Varies widely; hijiki also contains arsenic

· Ecological note: Sustainably harvested seaweed has low environmental impact. However, overharvesting and cultivation practices vary.

· Practical guidance:

· If using seaweed regularly, choose varieties with moderate iodine content (wakame, nori, dulse) and limit intake.

· Avoid regular consumption of kelp (kombu) unless iodine status is known and intake carefully measured.

· Soaking and cooking reduces iodine content (leaches into water).

· Iodised salt: Not a "plant" but a fortified food. It is the most reliable, cost‑effective, and ecologically acceptable way to ensure iodine adequacy in most populations.

· Guidance: Use iodised salt in cooking and at the table. Store in a cool, dark, dry container; iodine volatility increases with humidity and heat.

· Amount: 1/2 teaspoon (approx 2.5 g) of iodised salt provides about 75–100 mcg iodine (assuming 30–40 mg/kg).

· Cranberries: Contain some iodine; variable.

· Potatoes with skin: Small amounts, soil‑dependent.

· Legumes, grains, fruits, vegetables: Generally very low (<10 mcg per serving) unless grown in iodine‑replete coastal soils or irrigated with iodine‑rich water. Not reliable sources.

Fungi and algae:

· Mushrooms: Low iodine content unless grown in iodine‑enriched substrate (rare).

· Spirulina, chlorella: Contain minimal iodine; not reliable sources.

Biotechnology / fermentation‑derived:

· Iodised salt is the primary example of fortification.

· Iodine‑enriched yeast: Not commercially significant.

Dairy and eggs:

· Milk, yoghurt, cheese: Good sources in regions where dairy cattle are given iodine‑supplemented feed or iodine‑containing disinfectants (teat dips) are used. Content highly variable.

· Eggs: Iodine content depends on hen feed. Eggs from hens fed iodine‑enriched feed can provide 20–30 mcg per egg.

· Ecological note: Dairy has higher carbon footprint than plant sources; eggs intermediate.

Meat, fish, poultry (lowest priority):

· Fish and seafood: Excellent iodine sources – cod, haddock, tuna, shrimp, oysters. However:

· Ecological cost: overfishing, bycatch, habitat destruction, ocean pollution (mercury, PCBs)

· Not aligned with plant‑based hierarchy

· If consumed occasionally, choose low‑trophic, sustainably sourced species (e.g., sardines, mackerel, farmed shellfish with responsible practices)

· Meat and poultry: Low to moderate iodine content; animal feed often supplemented.

Practical dietary approach to optimise iodine intake (with ecological hierarchy):

1. Use iodised salt daily. This is the single most important and sustainable strategy. Choose iodised salt over non‑iodised gourmet salts.

2. If you avoid salt for medical reasons (hypertension, heart failure), or use only non‑iodised salt, you must supplement with 150 mcg iodine daily (as potassium iodide).

3. Incorporate moderate amounts of lower‑iodine seaweed (nori, wakame, dulse) if desired, but do not rely on them as primary source.

4. Avoid regular consumption of kelp (kombu) and kelp supplements due to unpredictability and toxicity risk.

5. If you consume dairy, choose organic or locally produced if available – iodine content may be higher in some regions. But this is not a primary strategy.

6. Limit or avoid high‑iodine fish (tuna, swordfish) due to mercury and ecological concerns.

7. Pregnancy and breastfeeding: Supplement. Do not rely on diet alone in iodine‑deficient regions.

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6. How soon can one expect improvement and the ideal time frame to retest

Iodine repletion:

· Urinary iodine concentration: Responds within days to increased intake. Spot urine levels fluctuate; 24‑hour collection more reliable.

· Thyroid function (TSH, FT4):

· In mild deficiency with normal thyroid function, no change expected.

· In hypothyroid deficiency, levothyroxine (with or without iodine) normalises TSH over 6–8 weeks.

· Iodine alone in simple goitre: Reduction in goitre size may be observed over 6–12 months.

· Goitre resolution: Takes months to years; complete resolution may not occur if longstanding with fibrosis.

Iodine excess:

· After discontinuing supplements: Urinary iodine declines within days to weeks.

· Thyroid function: May normalise over weeks to months depending on the underlying condition.

· Iodine‑induced hypothyroidism: Often transient; recovery over 2–6 weeks after iodine withdrawal.

· Iodine‑induced hyperthyroidism: May persist longer; requires treatment.

Retesting indications:

· Deficiency: Recheck urinary iodine and TSH 3–6 months after initiating supplementation or dietary change.

· Excess: Recheck urinary iodine and thyroid function at 1 month, then 3 months until normalised.

· Pregnancy: Monitor TSH each trimester if iodine supplementation initiated; urinary iodine not routinely repeated.

· Chronic conditions affecting iodine status: Annual monitoring if stable; more frequent if clinically changing.

· Not indicated for routine population screening in asymptomatic individuals without risk factors.

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Conclusion

Iodine is the substrate of thought – the raw material from which the thyroid crafts the hormones that fuel every cell, every synapse, every heartbeat. Its story is written in the soil and the sea, in the goitres of mountain villagers and the cognitive potential of their children. Two billion people still live with the weight of deficiency, their brains and bodies subtly starved. Yet iodine is also the element of paradox: a little nurtures, a little more injures. The thyroid, that most sensitive of organs, detects the slightest excess and responds with autoimmunity or autonomy. The blood test – or more properly, the urinary iodine concentration – reveals where we stand on this continuum. But numbers alone are not enough; they must be paired with TSH, with antibodies, with the clinical whisper of fatigue or the thunder of tachycardia. Treatment is precise: iodised salt for the many, measured supplements for the few, and for those in whom iodine is medicine turned poison, withdrawal and watchful waiting. The ecological path honours the mountain communities by supporting universal salt iodisation, respects the ocean by choosing seaweed wisely, and recognises that a single teaspoon of iodised salt holds more preventive power than all the kelp capsules in the pharmacy. Iodine teaches us that the smallest quantities carry the greatest responsibilities, and that the health of nations can hang on a grain of salt.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

This approach reflects ecological responsibility, antibiotic stewardship, and the urgent need to reduce the environmental footprint of dietary recommendations. In the case of iodine, iodised salt (a fortified / biotechnological product) is the preferred, most reliable, and most ecologically sustainable strategy for ensuring adequate intake, followed by moderate consumption of lower‑iodine seaweeds. Animal sources are not required and are ecologically costly.

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