Prevalence of Thyroid Dysfunction in Postpartum Women With Suboptimal Iodine and Selenium and Adequate Iron Status

Ying Jin; Jane Coad; Shao J. Zhou; Sheila Skeaff; Thiagarajah Ramilan; Louise Brough


Clin Endocrinol. 2021;95(6):873-881. 

In This Article

Abstract and Introduction


Objective: Postpartum women experience thyroid dysfunction at twice the prevalence of the general population. Adequate biosynthesis of thyroid hormones depends on three trace elements: iodine, selenium and iron. This study aimed to investigate thyroid dysfunction within a cohort of women at six months postpartum in relation to iodine, selenium and iron status.

Design: This cross-sectional study was part of an observational longitudinal cohort Mother and Infant Nutrition Investigation; data obtained at six months postpartum are reported.

Subjects: Mother-infant pairs (n = 87) were recruited at three months postpartum and followed up at six months postpartum (n = 78).

Measurements: Thyroid hormones (free triiodothyronine, free thyroxine, thyroid-stimulating hormone) and thyroid peroxidase antibodies were measured. Urinary iodine concentration, breast milk iodine concentration, serum thyroglobulin, plasma selenium, serum ferritin and serum soluble transferrin receptors were determined. Nonparametric data were expressed as median (25th, 75th percentile).

Results: Thyroid dysfunction was found in 18% of women, and 4% of women had iron deficiency. Median urinary iodine concentration was 85 (43, 134) μg/L, median breast milk iodine concentration was 59 (39, 109) μg/L, and median serum thyroglobulin at 11.4 (8.6, 18.6) μg/L, indicating iodine deficiency. Median plasma selenium concentration was 105.8 (95.6, 115.3) μg/L. Women with marginally lower plasma selenium concentration were 1.12% times more likely to have abnormal TSH concentrations (p = .001).

Conclusions: There was a high prevalence of thyroid dysfunction. Plasma selenium concentration was the only significant predictor of the likelihood that women had thyroid dysfunction within this cohort, who were iodine deficient and mostly had adequate iron status. Strategies are required to improve both iodine and selenium status to better support maternal thyroid function.


Thyroid dysfunction occurring in the first year after parturition is defined as postpartum thyroiditis (PPT). In 2017, the American Thyroid Association reported the prevalence of PPT ranged from 1.1% to 16.7%.[1] Most women initially diagnosed with PPT have normal thyroid hormones concentrations by the end of their first postpartum year.[1] However, longitudinal follow-up studies have reported that between 12% and 30% of women developed permanent hypothyroidism three to five years after the original episode of PPT.[2] The highest incidence reported was 54% of Italian women living in an area of mild iodine deficiency who had persistent hypothyroidism at the end of first postpartum year.[3] Maternal thyroid dysfunction has been linked to the development of postnatal depression,[4] is weakly associated with reduced breast milk production and milk-ejection reflex ("let-down"),[1] and may impact on infant neurodevelopment.[5]

Iodine, selenium and iron are essential for the synthesis of thyroid hormones.[6] Iodine is an integral component of thyroid hormones, thyroxine (T4) and triiodothyronine (T3). Selenium is a component of the selenocysteine-containing protein, glutathione peroxidase (GPX), which protects cells from damage by neutralising the excessive hydrogen peroxide generated during thyroid hormone synthesis.[7] The deiodinases, which convert biologically inactive T4 into active T3, are selenoproteins.[7] Furthermore, the activity of thyroid peroxidase, a haem-dependent enzyme required for adequate synthesis of thyroid hormones, is impaired in iron deficiency.[7]

The interaction between selenium and iodine in synthesizing thyroid hormones is of particular concern within New Zealand due to dietary insufficiency of both nutrients.[8] Two New Zealand government initiatives aim to improve iodine status: the mandatory fortification of bread with iodised salt, introduced in 2009, and the provision of iodine supplements for all pregnant and lactating women introduced in 2010. Despite these initiatives, this population group continues to have suboptimal iodine intake and status.[9] Selenium deficiency could potentially aggravate the negative consequences of mild iodine deficiency in this vulnerable group.[8] Further, the iron status of postpartum women in New Zealand is rarely clinically determined, except in women who had significant blood loss during childbirth.

This study aimed to investigate thyroid dysfunction in a cohort of women at six months postpartum in relation to maternal iodine, selenium and iron status.