IODINE DEFICIENCY IN PREGNANCY
Increases thyroid volume and risk of goiter in the populationoverall and in pregnant women These effects can beprevented with iodine supplementation or iodine fortification ofsalt Serum thyroglobulin concentrations are positivelycorrelated with thyroid volume in iodine-deficient regions and mild to moderate iodine deficiency may be associated withelevated serum thyroglobulin concentrations in adults and chil-dren However, mild iodine deficiency is generally notassociated with major alterations in serum thyroid function duringpregnancy.There is evidence that maternal iodine supplementation im-proves some maternal thyroid indexes even in marginally iodine-deficient areas. Nine randomized controlled trials of the effectsof iodine supplementation on measures of thyroid function inpregnantwomenhavebeenconductedtodateinmildlytomoderately iodine-deficient regions; results from these trials aresummarized in Tables 1 and 2 of a recent systematic review byTaylor et al. . Three of 4 trials in which maternal serum thyro-globulin was assessed found lower concentrations in supple-mented women than in controls, and 3 of 5 trials in which maternalserum thyroid-stimulating hormone (TSH) was assessed foundlower concentrations in supplemented women than in controls.There is also evidence that excessive iodine supplementationduring pregnancy can increase serum TSH concentrations andthus have a negative impact on maternal thyroid function. In oneobservational study, pregnant women who self-reported ingestingsupplements containing.200mg I/d were found to be at in-creased risk of serum TSH elevation compared with womenwhose supplemental iodine intake was,100mg/d Anotherobservational study showed higher serum TSH concentrations inwomen with a supplemental iodine intake of 150mg/d starting inearly pregnancy compared with women who used iodized saltstarting 2 y before pregnancy and women without iodized salt oriodine supplement use Only 3 clinical trials have assessedneonatal thyroid function in the offspring of supplementedwomen compared with nonsupplemented women, and these didnot show any differences; results from the 3 trials are summa-rized in the systematic review by Taylor et al.
It is not clear to what extent mild maternal iodine deficiencyduring pregnancy influences child neurobehavioral development. Although 2 observational studies have reported that mildmaternal iodine deficiency during pregnancy is associated witheither lower child intelligence quotient or educational as-sessment scores, there is conflicting information from ob-servational studies with regard to the effects of maternal iodinesupplementation on child neurobehavioral development in areasof mild iodine deficiency. One observational study found thatsupplemental iodine at$150mg/d did not improve psychomotoror mental development in the infant offspring of either mildlyiodine-deficient or iodine-sufficient pregnant women and mayhave adversely affected these outcome measures , whereas 2other uncontrolled observational studies found a possible im-provement in psychomotor development, but not mental de-velopment, with prenatal supplementation . A randomizedclinical trial conducted in a region of mild to moderate iodinedeficiency evaluated psychomotor development in the offspring of3 groups of pregnant women; 2 of the groups received supple-mental iodine at either 200 or 300mg/d and all of the groups wereadvised to use iodized salt in cooking
On the basis of available information, several medical andpublic health advisory groups have recommended iodine sup-plementation for women who are pregnant, lactating, or planninga pregnancy but these recommendations have not beenwidely adopted to date in most regions . Apparently,many government health authorities have been reluctant to makebroad recommendations for iodine supplementation in the ab-sence of definitive evidence from randomized clinical trials
EFFECTS OF IODINE EXCESS IN PREGNANCY
Excessive iodine intake can cause alterations in thyroid functionin susceptible individuals . In normal individuals, high iodineexposure can cause transient inhibition of thyroid hormone syn-thesis by a mechanism known as the acute Wolff-Chaikoff effect(49). Typically, the thyroid “escapes” from the acute Wolff-Chaikoff effect within a few days through downregulation of theiodide transporter in thyroid cells, and normal thyroid hormonesynthesis resumes (50, 51).Failure of the “escape” can result in iodine-induced hypo-thyroidism (51). This is seen most frequently in those withHashimoto thyroiditis. The ability to fully escape from the acuteWolff-Chaikoff effect does not mature untilw36 wk of gestation,and fetal hypothyroidism may develop in the setting of a largeiodine load even if maternal thyroid function is maintained .By contrast, iodine-induced hyperthyroidism represents a failureof the acute Wolff-Chaikoff effect. It occurs most frequently inthose with nodular goiters, which are more common in iodine-deficient regions.The above effects have been described for very high iodineexposures associated with medical or diagnostic doses. Populationincreases in dietary iodine intake are found to be associated withincreased prevalence of thyroid autoimmunity A recentcross-sectional study conducted in China showed a U-shapedrelation between thyroid function and UIC among 7190 women inthe first trimester of pregnancy, with the lowest serum TSH andthyroglobulin values associated with UICs of 150–249mg/L (56).For pregnant women, the Institute of Medicine recommends aniodine upper limit of 1100mg/d (57), whereas the WHO moreconservatively recommends an upper limit of 500mg/d (58). Thedata from the above-described Chinese study suggest that theInstitute of Medicine’s recommended 1100mg/d upper limit istoo high
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