I is required for the synthesis of thyroid hormones. These hormones, in tur
n, are required for brain development, which occurs during fetal and early
postnatal life. The present paper reviews the impact of I deficiency (1) on
thyroid function during pregnancy and in the neonate, and (2) on the intel
lectual development of infants and children. All extents of I deficiency (b
ased on I intake (mu g/d); mild 50-99, moderate 20-49, severe < 20) affect
the thyroid function of the mother and neonate, and the mental development
of the child. The damage increases with the extent of the deficiency, with
overt endemic cretinism as the severest consequence. This syndrome combines
irreversible mental retardation, neurological damage and thyroid failure.
Maternal hypothyroxinaemia during early pregnancy is a key factor in the de
velopment of the neurological damage in the cretin. Se deficiency superimpo
sed on I deficiency partly prevents the neurological damage, but precipitat
es severe hypothyroidism in cretins. I deficiency results in a global loss
of 10-15 intellectual quotient points at a population level, and constitute
s the world's greatest single cause of preventable brain damage and mental
retardation.