Thyroid function in human pregnancy: V. Incidence of maternal serum low butanol-extractable iodines and of normal gestational TBG and TBPA capacities; Retardation of 8-month-old infants

doi:10.1016/0002-9378(69)90644-9

American Journal of Obstetrics and Gynecology

Volume 104, Issue 6, 15 July 1969, Pages 898-908

https://doi.org/10.1016/0002-9378(69)90644-9 Get rights and content

Abstract

Although irreversible damage to the fetal central nervous system has been attributed to intrauterine thyroid deficiency, the incidence, in uncomplicated human pregnancies, of low maternal circulating thyroxine-like compounds is not available. One or more serum butanol-extractable iodines (BEI) were measured during 1,394 pregnancies of clinic registrants at Providence Lying-In Hospital; serum thyroxine-binding globulin (TBG) and thyroxine-binding prealbumin capacities (TBPA) were measured during 375 pregnancies. Eight-month-old infants were examined with the COLR form of Bayley's scales of mental and motor development. During 173 of 1,394 pregnancies BEI failed to rise to normally increased gestational concentrations but TBG and TBPA were normal gestationally during 89 of 105 of these pregnancies; in contrast only in 48 pregnancies were hyperthyroidism, high BEI, or other thyroid dysfunction diagnosed. Eighty-one per cent of 26 infants of women, given adequate Proloid after 2 low BEI, were classified “normal,” approximately the same per cent as for infants of euthyroid women; but only 48 per cent of 56 infants of women with 2 low BEI not given adequate thyroid replacement therapy were “normal.”

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Therefore the indiscriminate recommendation to increase iodine supply in normal pregnancies could do more harm if the population is iodine sufficient. If the studied population bears similarities to those described by Man [33] (Fig. 1), i.e. premature babies with hypothyroxinemia, the negative results on IQ can be similar [53]. The question of hypothyroxinemia leads us to the way on how to detect such cases.
Since the 1960s hypothyroidism together with iodine deficiency have been considered to be a principal determinant of cognition development. Following iodine supplementation programs and improved treatment options for hypothyroidism this relation might not be valid in 2015. On the other hand neurosciences have added different inputs also related to cognition.
We will examine the characteristics of the original and current publications on thyroid function and cognition and also add some general determinants of intelligence and cognition. One central issue for us is the relation of stress to cognition knowing that both physical and psychological stress, are frequent elements in subjects with thyroid dysfunction. We have considered a special type of stress called pre-natal stress which can influence cognitive functions. Fear and anxiety can be intermingled requiring mechanisms of fear extinction.
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^☆: Supported in part by Public Health Service Research Grants AM-04890-01, -02 from The National Institute of Arthritis and Metabolic Diseases, which was transferred to HD-00415-03,-04, -05 from the National Institute of Child Health and Human Development; HD-01821-01, -02 from the National Institute of Child Health and Human Development; and by a grant from the Warner-Lambert Research Institute.

^☆☆: Presented in part at the Annual Meeting of the American Thyroid Association, Washington, D. C., Oct. 10–12, 1968.

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Thyroid function in human pregnancy: V. Incidence of maternal serum low butanol-extractable iodines and of normal gestational TBG and TBPA capacities; Retardation of 8-month-old infants☆,☆☆

Abstract

J. Pediat

Am. J. Obst. & Gynec

J. Pediat

Am. J. Obst. & Gynec

Am. J. Obst. & Gynec

Am. J. Obst. & Gynec

J. Chron. Dis

J. Michigan State M. Soc

Obst. & Gynec

Am. J. Dis. Child