Iodine deficiency in pregnancy and it's effects on offspring

assorted studies~ 

http://www.eje-online.org/cgi/content/full/159/4/439

At a meeting of experts held on January 24 and 25, 2005, at the Headquarters of the World Health Organization in Geneva, the increasing evidence was evaluated that suggested that previous recommendations on iodine nutrition during pregnancy and breastfeeding should be reviewed (1). In this meeting, the conclusion was reached that women should ingest at least 250 µg I/day during pregnancy and breastfeeding, to prevent possible defects in fetal brain development. Present-day reality shows that we are far from accomplishing this (2), not only in Western Europe (3), but also probably in North America (4).

The present concern about insufficient iodine nutrition during pregnancy and breastfeeding is related to the increasing evidence that an insufficient iodine intake negatively and irreversiblyaffects the psychoneurointellectual development of the fetus (5, 6, 7, 8, 9, 10), especially when there is a deficiency during the first trimester.

The present report assembles the results of an epidemiological study carried out in the Spanish Autonomous Community of Extremadura, aimed at evaluating the state of iodine nutrition of pregnant women, with special attention to their condition during the first trimester.

Iodine deficiency in the area of Las Hurdes Altas (El Gasco, Fragosa, Martilandrán) of Extremadura was so frequent and severe that after the visit of the King of Spain, Alfonso XIII, several doctors were sent to live in the most affected villages. A successful iodine prophylaxis in the schoolchildren and in pregnant women was initiated, unfortunately interrupted with the onset of the Spanish civil war. Epidemiological studies in this area were again undertaken in the late sixties with initial results from two decades being published in 1981 (11). The prevalence of goiter in schoolchildren was initially very high, with an overall frequency of 86%; urinary iodine (UI) was <20 µg/l in 71% of the schoolchildren. Circulating thyroxine (T₄) was less than 78 nmol/l in 46% of them. Their somatic development was retarded and so was their mental development (12, 13, 14).

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http://jcem.endojournals.org/cgi/content/abstract/89/12/6054?ijkey=26de5acd94...

Attention Deficit and Hyperactivity Disorders in the Offspring of Mothers Exposed to Mild-Moderate Iodine Deficiency: A Possible Novel Iodine Deficiency Disorder in Developed Countries

Dipartimento Clinico-Sperimentale di Medicina e Farmacologia-Sezione di Endocrinologia (F.V., V.P.L.P., M.M., G.S., M.G.C., F.M., M.A.V., F.T.), Dipartimento di Scienze Pediatriche-Sezione di Neuropsichiatria Infantile (M.S., G.T., A.C.), and Dipartimento di Diagnostica di Laboratorio-Servizio di Biochimica Clinica (A.A.), University of Messina, Messina 98125, Italy

Address all correspondence and requests for reprints to: Prof. Francesco Vermiglio, M.D., Cattedra di Endocrinologia, Policlinico Universitario, Via Consolare Valeria 98125 Messina, Italy. E-mail: francesco.vermiglio@unime.it.

Over a period of almost 10 yr, we carried out a prospective study of the neuropsychological development of the offspring of 16 women from a moderately iodine-deficient area (area A) and of 11 control women from a marginally iodine-sufficient area (area B) whose thyroid function had been monitored during early gestation.

Attention deficit and hyperactivity disorder (ADHD) was diagnosed in 11 of 16 area A children (68.7%) but in none from area B. Total intelligence quotient score was lower in area A than in area B children (92.1 ± 7.8 vs. 110 ± 10) and in ADHD children when compared with both non-ADHD children from the same area and control children (88.0 ± 6.9 vs. 99.0 ± 2.0 and 110 ± 10, respectively). Seven of 11 ADHD children (63.6%) were born to the seven of eight area A mothers who became hypothyroxinemic at early gestation, whereas only one of five non-ADHD children was born to a woman who was hypothyroxinemic at 20 wk of gestation.

So far, a similar prevalence of ADHD has been reported only in children with generalized resistance to thyroid hormones. This might suggest a common ADHD pathogenetic mechanism consisting either of reduced sensitivity of the nuclear receptors to thyroid hormone (generalized resistance to thyroid hormones) or reduced availability of intracellular T₃ for nuclear receptor binding. The latter would be the ultimate consequence of maternal hypothyroxinemia (due to iodine deficiency), resulting in a critical reduction of the source of the intracellular T₃available to the developing fetal brain.

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http://www.nejm.org/doi/full/10.1056/NEJM199412293312610

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The influence of iodine deficiency during pregnancy 

on child neurodevelopment 0-24 months of age in 

East Java, Indonesia 

http://www.neurology-asia.org/articles/20052_113.pdf

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http://www.ncbi.nlm.nih.gov/pubmed

1. Am J Clin Nutr. 2009 Nov;90(5):1264-71. Epub 2009 Sep 2.

Iodine supplementation improves cognition in mildly iodine-deficient children.

Gordon RC, Rose MC, Skeaff SA, Gray AR, Morgan KM, Ruffman T.

Department of Human Nutrition, University of Otago, Dunedin, New Zealand.

BACKGROUND: The effects of severe iodine deficiency during critical periods of
brain development are well documented. There is little known about the
consequences of milder forms of iodine deficiency on neurodevelopment.
OBJECTIVE: The objective was to determine whether supplementing mildly
iodine-deficient children with iodine improves cognition.
DESIGN: A randomized, placebo-controlled, double-blind trial was conducted in 184
children aged 10-13 y in Dunedin, New Zealand. Children were randomly assigned to
receive a daily tablet containing either 150 microg I or placebo for 28 wk.
Biochemical, anthropometric, and dietary data were collected from each child at
baseline and after 28 wk. Cognitive performance was assessed through 4 subtests
from the Wechsler Intelligence Scale for Children.
RESULTS: At baseline, children were mildly iodine deficient [median urinary
iodine concentration (UIC): 63 microg/L; thyroglobulin concentration: 16.4
microg/L]. After 28 wk, iodine status improved in the supplemented group (UIC:
145 microg/L; thyroglobulin: 8.5 microg/L), whereas the placebo group remained
iodine deficient (UIC: 81 microg/L; thyroglobulin: 11.6 microg/L). Iodine
supplementation significantly improved scores for 2 of the 4 cognitive subtests
[picture concepts (P = 0.023) and matrix reasoning (P = 0.040)] but not for
letter-number sequencing (P = 0.480) or symbol search (P = 0.608). The overall
cognitive score of the iodine-supplemented group was 0.19 SDs higher than that of
the placebo group (P = 0.011).
CONCLUSIONS: Iodine supplementation improved perceptual reasoning in mildly
iodine-deficient children and suggests that mild iodine deficiency could prevent 
children from attaining their full intellectual potential. The trial was
registered with the Australia New Zealand Clinical Trials Register as
ACTRN12608000222347.


PMID: 19726593 [PubMed - indexed for MEDLINE]

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MOTHERLODE of links here, in "Aunt Cathy’s Guide to Nutrition: New Attention to an Old Problem:  Iodine Deficiency in  Pregnancy and Lactation  

Cathy Breedon PhD, RD, CSP, FADA  

Clinical and Metabolic Nutrition Specialist 

MeritCare Medical Center Dept. of Pediatrics 

http://tinyurl.com/4r57mgr

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http://www.ncbi.nlm.nih.gov/pubmed

1. Br J Nutr. 2008 Jun;99(6):1178-81.

Amniotic fluid iodine concentrations do not vary in pregnant women with varying
iodine intake.

García-Fuentes E, Gallo M, García L, Prieto S, Alcaide-Torres J, Santiago P,
Velasco I, Soriguer F.

Servicio de Endocrinología y Nutrición, Hospital Universitario Carlos Haya,
Málaga, Spain. edugf1@eresmas.com

Iodine deficiency is an important clinical and public health problem. Its
prevention begins with an adequate intake of iodine during pregnancy.
International agencies recommend at least 200 microg iodine per d for pregnant
women. We assessed whether iodine concentrations in the amniotic fluid of healthy
pregnant women are independent of iodine intake. This cross-sectional,
non-interventional study included 365 consecutive women who underwent
amniocentesis to determine the fetal karyotype. The amniocentesis was performed
with abdominal antisepsis using chlorhexidine. The iodine concentration was
measured in urine and amniotic fluid. The study variables were the intake of
iodized salt and multivitamin supplements or the prescription of a KI supplement.
The mean level of urinary iodine was 139.0 (SD 94.5) microg/l and of amniotic
fluid 15.81 (SD 7.09) microg/l. The women who consumed iodized salt and those who
took a KI supplement had significantly higher levels of urinary iodine than those
who did not (P = 0.01 and P = 0.004, respectively). The urinary iodine levels
were not significantly different in the women who took a multivitamin supplement 
compared with those who did not take this supplement, independently of iodine
concentration or multivitamin supplement. The concentrations of iodine in the
amniotic fluid were similar, independent of the dietary iodine intake. Urine and 
amniotic fluid iodine concentrations were weakly correlated, although the
amniotic fluid values were no higher in those women taking a KI supplement. KI
prescription at recommended doses increases the iodine levels in the mother
without influencing the iodine levels in the amniotic fluid.


PMID: 18205989 [PubMed - indexed for MEDLINE]