Share this article on:

Iodine Intake and Maternal Thyroid Function During Pregnancy

Rebagliato, Marisaa,b; Murcia, Marioa,c; Espada, Mercedesd; Álvarez-Pedrerol, Mara,e; Bolúmar, Franciscoa,f; Vioque, Jesúsa,b; Basterrechea, Mikela,g; Blarduni, Elizabethh; Ramón, Rosaa,c; Guxens, Mónicaa,e; Foradada, Carles M.i; Ballester, Ferrána,c; Ibarluzea, Jesúsa,g; Sunyer, Jordia,e,j

doi: 10.1097/EDE.0b013e3181c1592b
Endocrine: Original Article

Background: An adequate iodine intake during pregnancy is essential for the synthesis of maternal thyroid hormones and normal brain development in the fetus. Scant evidence is available on the effects and safety of iodine supplementation during pregnancy in areas with adequate or mildly deficient iodine intake. We examined the association of maternal iodine intake and supplementation with thyroid function before 24 weeks of gestation in population-based samples from 3 different areas in Spain.

Methods: A cross-sectional study of 1844 pregnant women (gestational age range 8–23 weeks) was carried out in 3 areas in Spain (Guipúzcoa, Sabadell, Valencia), during the period 2004–2008. We measured levels of free thyroxine and thyroid-stimulating hormone (TSH) in serum, iodine in a spot urine sample, and questionnaire estimates of iodine intake from diet, iodized salt and supplements. Adjusted associations were assessed by multiple linear regression and logistic regression analyses.

Results: There was an increased risk of TSH above 3 μU/mL in women who consumed 200 μg or more of iodine supplements daily compared with those who consumed less than 100 μg/day (adjusted odds ratio = 2.5 [95% confidence interval = 1.2 to 5.4]). We observed no association between urinary iodine and TSH levels. Pregnant women from the area with the highest median urinary iodine (168 μg/L) and highest supplement coverage (93%) showed the lowest values of serum free thyroxine. (geometric mean = 10.09 pmol/L [9.98 to 10.19]).

Conclusions: Iodine supplement intake in the first half of pregnancy may lead to maternal thyroid dysfunction in iodine-sufficient or mildly iodine-deficient populations.

From the aCentro de Investigación Biomédica en Red de Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; bDepartment of Public Health, Miguel Hernández University, Ctra Alicante-Valencia, San Juan de Alicante, Spain; cDivision of Environment and Health, Valencian School for Health Studies-EVES, Valencian Center for Research on Public Health-CSISP, Valencia, Spain; dDepartamento de Sanidad Gobierno Vasco, Laboratorio Normativo de Salud Pública, María Díaz de Haro, Bilbao, Spain; eCentre for Research in Environmental Epidemiology, Barcelona, Spain; fDepartamento de Ciencias Sanitarias y Médico-Sociales, Alcalá University, Ctra Madrid-Barcelona, Alcalá de Henares, Madrid, Spain; gDepartamento de Sanidad Gobierno Vasco, Subdirección de Salud Pública de Guipúzcoa, Avenida de Navarra, San Sebastián, Spain; hDepartment of Pediatrics, Hospital Zumarraga, Osakidetza, Barrio Argixao s/n, Zumárraga, Spain; iDepartment of Obstetrics and Gynecology, Hospital Parc Taulí, Sabadell, Spain; and jDepartment of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain.

Submitted 17 December 2008; accepted 15 September 2009.

Supported by grants from Instituto de Salud Carlos III (Red INMA G03/176 and CB06/02/0041), the Spanish Ministry of Health (FIS 03/1615, FIS 04/1509, FIS 04/1436, FIS 05/1079, FIS 06/1213, FIS06/0867), Ministerio Educación y Ciencia (SAF2002-03508), the Generalitat de Catalunya-CIRIT 1999SGR 00241, Departamento de Sanidad-Gobierno Vasco 2005111093, and Diputación Foral de Gipuzkoa 06/004.

Correspondence: Marisa Rebagliato, Miguel Hernández University, Department of Public Health, Ctra Alicante-Valencia, Km 87, 03550 San Juan de Alicante, Spain. E-mail:

© 2010 Lippincott Williams & Wilkins, Inc.