OBJECTIVES: Normal brain development is highly dependent on adequate levels of iodine and thyroid hormone. It has been suggested that Attention Deficit Hyperactivity Disorder (ADHD) is the consequence of prenatal thyroidal endocrine disruption. The hypothesis was examined using neonatal thyroxine levels as a bio-marker of prenatal thyroid status and comparing it to subsequent development of ADHD. DESIGN AND METHODS: In a matched case-control study, cases were defined as children diagnosed with ADHD, while children born in the same hospital and tested on the same day served as matched controls. Conditional logistic regression analysis with unequal numbers of controls was performed. RESULTS: The neonatal thyroxine levels were within normal limits for each of the children who were subsequently diagnosed as having ADHD, and their distribution was no different from that of their controls. CONCLUSIONS: Children diagnosed with ADHD do not demonstrate prenatal thyroidal dysfunction as reflected in the newborn thyroxine levels, therefore neonatal thyroxine levels are not a bio-marker for the subsequent development of ADHD.
OBJECTIVES: Normal brain development is highly dependent on adequate levels of iodine and thyroid hormone. It has been suggested that Attention Deficit Hyperactivity Disorder (ADHD) is the consequence of prenatal thyroidal endocrine disruption. The hypothesis was examined using neonatal thyroxine levels as a bio-marker of prenatal thyroid status and comparing it to subsequent development of ADHD. DESIGN AND METHODS: In a matched case-control study, cases were defined as children diagnosed with ADHD, while children born in the same hospital and tested on the same day served as matched controls. Conditional logistic regression analysis with unequal numbers of controls was performed. RESULTS: The neonatal thyroxine levels were within normal limits for each of the children who were subsequently diagnosed as having ADHD, and their distribution was no different from that of their controls. CONCLUSIONS:Children diagnosed with ADHD do not demonstrate prenatal thyroidal dysfunction as reflected in the newborn thyroxine levels, therefore neonatal thyroxine levels are not a bio-marker for the subsequent development of ADHD.
Authors: D Glinoer; P De Nayer; F Delange; M Lemone; V Toppet; M Spehl; J P Grün; J Kinthaert; B Lejeune Journal: J Clin Endocrinol Metab Date: 1995-01 Impact factor: 5.958
Authors: V J Pop; E de Vries; A L van Baar; J J Waelkens; H A de Rooy; M Horsten; M M Donkers; I H Komproe; M M van Son; H L Vader Journal: J Clin Endocrinol Metab Date: 1995-12 Impact factor: 5.958
Authors: Emily Oken; Lewis E Braverman; Deborah Platek; Marvin L Mitchell; Stephanie L Lee; Elizabeth N Pearce Journal: J Clin Endocrinol Metab Date: 2008-11-25 Impact factor: 5.958
Authors: Samantha S M Drover; Gro D Villanger; Heidi Aase; Thea S Skogheim; Matthew P Longnecker; R Thomas Zoeller; Ted Reichborn-Kjennerud; Gun P Knudsen; Pål Zeiner; Stephanie M Engel Journal: Epidemiology Date: 2019-01 Impact factor: 4.822