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Attention Deficit and Hyperactivity Disorders in the Offspring of Mothers Exposed to Mild-Moderate Iodine Deficiency: A Possible Novel Iodine Deficiency Disorder in Developed Countries

Dipartimento Clinico-Sperimentale di Medicina e Farmacologia-Sezione di Endocrinologia (F.V., V.P.L.P., M.M., G.S., M.G.C., F.M., M.A.V., F.T.), Dipartimento di Scienze Pediatriche-Sezione di Neuropsichiatria Infantile (M.S., G.T., A.C.), and Dipartimento di Diagnostica di Laboratorio-Servizio di Biochimica Clinica (A.A.), University of Messina, Messina 98125, Italy

Address all correspondence and requests for reprints to: Prof. Francesco Vermiglio, M.D., Cattedra di Endocrinologia, Policlinico Universitario, Via Consolare Valeria 98125 Messina, Italy. E-mail: francesco.vermiglio{at}unime.it.

Over a period of almost 10 yr, we carried out a prospective study of the neuropsychological development of the offspring of 16 women from a moderately iodine-deficient area (area A) and of 11 control women from a marginally iodine-sufficient area (area B) whose thyroid function had been monitored during early gestation.

Attention deficit and hyperactivity disorder (ADHD) was diagnosed in 11 of 16 area A children (68.7%) but in none from area B. Total intelligence quotient score was lower in area A than in area B children (92.1 ± 7.8 vs. 110 ± 10) and in ADHD children when compared with both non-ADHD children from the same area and control children (88.0 ± 6.9 vs. 99.0 ± 2.0 and 110 ± 10, respectively). Seven of 11 ADHD children (63.6%) were born to the seven of eight area A mothers who became hypothyroxinemic at early gestation, whereas only one of five non-ADHD children was born to a woman who was hypothyroxinemic at 20 wk of gestation.

So far, a similar prevalence of ADHD has been reported only in children with generalized resistance to thyroid hormones. This might suggest a common ADHD pathogenetic mechanism consisting either of reduced sensitivity of the nuclear receptors to thyroid hormone (generalized resistance to thyroid hormones) or reduced availability of intracellular T₃ for nuclear receptor binding. The latter would be the ultimate consequence of maternal hypothyroxinemia (due to iodine deficiency), resulting in a critical reduction of the source of the intracellular T₃ available to the developing fetal brain.

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