This 2025 state-of-the-art review from researchers in Malaysia and New Zealand synthesizes current global evidence on iodine nutrition during pregnancy and lactation, with a specific focus on child cognitive outcomes. It covers the physiology of iodine in pregnancy and lactation, the global prevalence and consequences of both deficiency and excess, a critical appraisal of intervention trial data, and directions for future research.
The central conclusion is a U-shaped association: children born to mothers with the lowest and highest iodine intakes both perform worse on neurodevelopmental assessments than those born to mothers in the adequate range. This framing is important for clinical practice, where iodine is often discussed primarily as a deficiency problem.
Iodine is the essential substrate for thyroid hormone synthesis. T3 and T4 are not optional nutrients for fetal brain development: they drive neurogenesis, neuronal migration, synaptogenesis, and myelination. Without them, brain formation is compromised in ways that cannot be fully reversed after the fact.
During pregnancy, maternal iodine requirements increase by roughly 50% due to three simultaneous demands: elevated glomerular filtration rate increases renal iodine clearance, maternal thyroid hormone production rises to support both mother and fetus, and the fetus requires direct iodine transfer, particularly from the second trimester onward when its own thyroid begins to function.
The first trimester is the most critical window. Until approximately week 12, the fetal thyroid does not produce its own hormones at all. The developing brain is entirely dependent on maternal T4 during this period. Even subclinical maternal hypothyroidism or isolated hypothyroxinaemia (low free T4 with normal TSH) during early gestation can impair fetal neurodevelopment in ways that routine thyroid screening may not detect, since TSH is a relatively insensitive marker of population iodine status.
The demands do not end at birth. Iodine is actively concentrated into breast milk via the sodium/iodide symporter in the mammary gland. The recommended intake during lactation is 250 µg/day, reflecting the need to maintain breast milk iodine concentrations ideally between 100 and 200 µg/L. Iodine deficiency during the first six months of life can severely impair cognitive and psychomotor development, and these effects may be irreversible even if iodine status is corrected later.
Formula-fed infants are also at risk if formula iodine content is inadequate. Breastfeeding provides no protection if the mother herself is iodine deficient. This makes lactating women a population requiring the same level of monitoring attention as pregnant women, despite receiving considerably less clinical focus.
The tolerable upper intake levels are substantially higher than typical dietary intakes for most populations. However, as the cognitive outcome data make clear, staying well below the upper limit does not guarantee optimal neurodevelopmental outcomes. The PINK cohort from Australia found cognitive harm beginning at intakes above approximately 370 µg/day, which is well below the formal upper limit of 1100 µg/day. The upper limit reflects safety from thyroid dysfunction, not necessarily from neurodevelopmental risk.
Based on PINK cohort (Australia) data. Inflection points approximate. Individual studies vary.
The PINK cohort study of 794 Australian pregnant women found that children in both the lowest quartile (under 220 µg/day) and highest quartile (over 391 µg/day) of maternal iodine intake during pregnancy had significantly poorer cognitive and language outcomes compared to children of mothers in the middle range. A follow-up analysis in the same cohort identified approximate inflection points: cognitive scores declined at intakes below 185 µg/day and again above 370 µg/day. Language scores were adversely affected above 350 µg/day.
This curvilinear pattern has now been observed in multiple cohorts across different countries and contexts, giving it increasing biological plausibility:
The Bangladesh data add an important nuance: elevated iodine status in the children themselves at ages 5 and 10 was not associated with cognitive differences. Only the prenatal period of excess appeared harmful. This points to the gestational window as the period of greatest vulnerability to iodine excess, not simply high iodine status in general.
The primary pathway through which excess iodine causes harm is disruption of thyroid hormone synthesis, via a process called the Wolff-Chaikoff effect. When the thyroid is acutely flooded with excess iodine, it temporarily shuts down hormone production by inhibiting thyroid peroxidase (TPO), the enzyme responsible for iodine organification. In most healthy adults, the thyroid escapes this suppression within 24 to 48 hours by downregulating the sodium/iodide symporter, reducing intrathyroidal iodine levels and restoring normal synthesis.
The fetus and neonate cannot do this reliably. Their thyroid glands are functionally immature throughout much of gestation and into the neonatal period. Failure to escape from iodine-induced suppression can lead to fetal or neonatal hypothyroidism, which, if unrecognized, has irreversible consequences for neurodevelopment.
Women with underlying thyroid autoimmunity, latent Hashimoto’s thyroiditis, or a history of chronic iodine deficiency are at particular risk, as thyroidal autoregulation is already compromised in these individuals. Even modest supplementation can trigger thyroid dysfunction in this subgroup. During lactation, excessive maternal iodine intake increases breast milk iodine concentration, potentially overwhelming the neonate’s immature thyroid.
Despite the strong observational evidence linking maternal iodine status to cognitive outcomes, the intervention trial data are remarkably inconsistent. Of five published randomized or controlled trials examining iodine supplementation during pregnancy and child neurodevelopment, only one (Velasco et al., Spain, 2009) found a significant benefit: a 6.1-point improvement in the Psychomotor Development Index at two years in children of mothers supplemented with 300 µg/day from the first trimester. The remaining four trials found no significant differences in cognitive, language, or motor outcomes.
| Study | Country | Dose / Timing | Age Assessed | Outcome |
|---|---|---|---|---|
| Velasco et al. (2009) | Spain | 300 µg KI from first trimester | 3 to 18 months | Higher PDI scores (p = 0.02) |
| Santiago et al. (2013) | Spain | Iodised salt vs 200 µg vs 300 µg KI | 6 to 18 months | No significant difference |
| Brucker-Davis et al. (2015) | France | 150 µg/day from first trimester | 2 years | No significant difference |
| Zhou et al. (2015) | Australia | 150 µg KI from second trimester | 18 months | No significant difference |
| Gowachirapant et al. (2009) | India / Thailand | 200 µg KI from first trimester | 5 to 6 years | No significant difference |
The authors propose several reasons for the null findings. Supplementation initiated during the second trimester may arrive too late to correct deficiency effects on first-trimester neurogenesis. Dose may be insufficient to restore depleted maternal stores. Some women in the supplemented groups may have already been iodine sufficient, in which case supplementation adds nothing and may even cause transient thyroid suppression. The review also notes that even a modest, abrupt increase in iodine intake within recommended levels can transiently suppress thyroid hormone synthesis during a critical developmental window.
The practical implication is that “start supplementing in the first trimester” is not a sufficient strategy on its own. Pre-conception iodine status assessment, and ideally pre-conception sufficiency, is the more defensible clinical goal.
Iodine deficiency in pregnancy is not a problem confined to low-income countries. Europe has some of the highest rates globally: an estimated 69% of pregnant European women have insufficient iodine intake. Notable examples from the review include Iran (97% of pregnant women with insufficient intake), Ukraine (96%), Turkey (90%), and Norway (90%), as well as the UK, where no mandatory salt iodisation program exists and a median UIC of 85 µg/L was documented in pregnant women. Even with supplementation, countries like Belgium and Denmark still fail to reach the WHO threshold of 150 µg/L median UIC in pregnant women.
In regions without accessible iodine-rich foods (inland or mountainous areas, countries with low seafood and dairy consumption), the gap is even wider. In mountainous Iran, 98% of first-trimester pregnant women had insufficient iodine intake versus 84% in lowland areas.
Iodine excess is primarily a concern in areas where drinking water contains naturally high iodine concentrations, particularly in coastal regions and areas affected by high rainfall or seawater intrusion. Multiple studies from China document pregnant women with urinary iodine concentrations substantially above 300 µg/L due to iodine-rich water supplies. One meta-analysis found that approximately 52% of pregnant women exceeded recommended intake levels globally, though with enormous variability across populations.
Kelp and seaweed are clinically important excess sources, particularly in populations consuming these foods regularly or using them as supplements. A single serving of some varieties of seaweed can deliver several times the recommended daily intake. This is relevant for patients who perceive seaweed-based products as health foods without understanding their iodine content.
The most actionable implication of this review is that iodine assessment and optimization should ideally begin before conception, not in the second trimester. The critical window for fetal brain development opens immediately after implantation. Waiting until a first prenatal visit to discuss iodine means the first trimester is already underway.
For patients in iodine-deficient regions or with low dietary iodine (limited dairy, seafood, and iodised salt use), supplementation at 150 to 250 µg/day is well-supported. For patients already consuming iodine-rich diets, supplementing with high-dose prenatal vitamins containing 150 to 220 µg of iodine on top of dietary intake warrants consideration of total iodine load.
Patients with Hashimoto’s thyroiditis, latent thyroid autoimmunity, or a history of postpartum thyroiditis warrant particular care. In these individuals, increasing iodine intake can precipitate hypothyroidism even at doses within the recommended range. Thyroid function monitoring alongside iodine supplementation is reasonable in this subgroup.
Patients who use seaweed supplements or consume large amounts of seaweed-based foods should be asked about this specifically. Iodine content in seaweed is highly variable and can be extraordinarily high; it is one of the more common unrecognized sources of excess intake in otherwise health-conscious patients.
Lactating women have the same recommended intake as pregnant women (250 µg/day WHO), yet receive far less clinical attention regarding iodine status. Breast milk iodine concentration directly tracks maternal iodine intake. An exclusively breastfed infant whose mother is iodine deficient is also iodine deficient. Continuing iodine supplementation through the breastfeeding period is warranted, and checking whether a patient’s postnatal supplement contains iodine (many do not) is a quick clinical check worth doing.
