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In developing mammals (including humans), a deficiency or excess of thyroid hormone (TH) in the developing brain during the fetal and neonatal periods can lead to morphological and functional abnormalities (Nunez et al., 1992; Pasquini & Adamo, 1994; Morreale de Escobar et al., 2004; Harakawa et al., 1989). The most severe form of hypothyroidism in human fetus and neonate is the syndrome of cretinism. Recent studies indicate that abnormalities in intelligence quotient (IQ) and other neuropsychological tests may be found in children of women with subclinical hypothyroidism during pregnancy (Haddow et al., 1999; Mitchell & Klein, 2004; Casey et al., 2005). Subtle health impairment and reduced socio-educational achievement are observed in young adults with congenital hypothyroidism identified by neonatal screening and subsequently treated (Leger et al., 2011). This suggests the inadequacy in the current strategy with neonatal screening – it may already be too late to secure normal neurological development. Studies of populations indicate that congenital hypothyroidism affects 1 in 3,000 to 4,000 newborns; twice as many females as males. A recent report showed that the incidence in the United States increased from ~ 1:4100 in 1987 to ~ 1:2400 in 2002 (Rastogi & LaFranchi, 2010; Harris & Pass, 2007). The causes for this change are not entirely clear even though the screening strategy may have contributed to the increase (Rastogi & LaFranchi, 2010).

A 3,3’-Diiodothyronine Sulfate Cross-Reactive Material (Compound W), a Potential Marker for Fetal Hypothyroidism