Maternal Iodine Status During Pregnancy Is Not Consistently Associated with Attention-Deficit Hyperactivity Disorder or Autistic Traits in Children.

The Generation R Study Group, Erasmus University Medical Centre, Rotterdam, Netherlands. Department of Internal Medicine, Academic Center For Thyroid Diseases, Erasmus University Medical Centre, Rotterdam, Netherlands. Department of Child and Adolescent Psychiatry/Psychology, Erasmus University Medical Centre-Sophia Children's Hospital, Rotterdam, Netherlands. ISGlobal, Barcelona, Spain. Department of Experimental and Health Sciences, Pompeu Fabra University, Barcelona, Spain. Spanish Consortium for Research on Epidemiology and Public Health (CIBERESP), Carlos III Health Institute, Madrid, Spain. Department of Nutritional Sciences, University of Surrey, Guildford, United Kingdom. BIODONOSTIA, Health Research Institute, Donostia-San Sebastián, Spain. Faculty of Psychology, University of the Basque Country (UPV/EHU), Donostia-San Sebastián, Spain. Basque Government Department of Health, Deputy Directorate of Public Health of Gipuzkoa, Donostia-San Sebastián, Spain. Epidemiology and Environmental Health Joint Research Unit, FISABIO-Jaume I University-University of València, Valencia, Spain. Hospital del Mar Research Institute (IMIM), Barcelona, Spain. Department of Social and Behavioral Science, Harvard TH Chan School of Public Health, Boston, MA, USA.

The Journal of nutrition. 2020;(6):1516-1528

Abstract

BACKGROUND Severe iodine deficiency during pregnancy can cause intellectual disability, presumably through inadequate placental transfer of maternal thyroid hormone to the fetus. The association between mild-to-moderate iodine deficiency and child neurodevelopmental problems is not well understood. OBJECTIVES We investigated the association of maternal iodine status during pregnancy with child attention-deficit hyperactivity disorder (ADHD) and autistic traits. METHODS This was a collaborative study of 3 population-based birth cohorts: Generation R (n = 1634), INfancia y Medio Ambiente (n = 1293), and the Avon Longitudinal Study of Parents and Children (n = 2619). Exclusion criteria were multiple fetuses, fertility treatment, thyroid-interfering medication use, and pre-existing thyroid disease. The mean age of assessment in the cohorts was between 4.4 and 7.7 y for ADHD symptoms and 4.5 and 7.6 y for autistic traits. We studied the association of the urinary iodine-to-creatinine ratio (UI/Creat) <150 μg/g-in all mother-child pairs, and in those with a urinary-iodine measurement at ≤18 weeks and ≤14 weeks of gestation-with the risk of ADHD or a high autistic-trait score (≥93rd percentile cutoff), using logistic regression. The cohort-specific effect estimates were combined by random-effects meta-analyses. We also investigated whether UI/Creat modified the associations of maternal free thyroxine (FT4) or thyroid-stimulating hormone concentrations with ADHD or autistic traits. RESULTS UI/Creat <150 μg/g was not associated with ADHD (OR: 1.2; 95% CI: 0.7, 2.2; P = 0.56) or with a high autistic-trait score (OR: 0.8; 95% CI: 0.6, 1.1; P = 0.22). UI/Creat <150 μg/g in early pregnancy (i.e., ≤18 weeks or ≤14 weeks of gestation) was not associated with a higher risk of behavioral problems. The association between a higher FT4 and a greater risk of ADHD (OR: 1.3; 95% CI: 1.0, 1.6; P = 0.017) was not modified by iodine status. CONCLUSIONS There is no consistent evidence to support an association of mild-to-moderate iodine deficiency during pregnancy with child ADHD or autistic traits.