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Iodine and the Body

 

Pregnancy

 

Smyth

 

Short-term changes in maternal and neonatal urinary iodine excretion.

Smyth PP, Smith DF, Sheehan S, Higgins M, Burns R, O'herlihy C.

Thyroid. 2007 Mar;17(3):219-22.

 

"Investigation of maternal urinary iodine (UI) excretion in the immediate antenatal and early postpartum periods showed a precipitous fall in median values from 93 mug/L antenatally to 36 mug/L at delivery subsequently rising to 49 mug/L and 63 mug/L at days 3 and 10 postpartum respectively. The fate of ingested iodine not appearing in the maternal urine is unknown but measurement of UI in babies born to nursing mothers suggested transfer from the mother with median neonatal values of 117 and 159 mug/L being recorded at days 3 and 10. While maternal UI seemed to relatively unaffected by breast feeding, median UI from breast feeding babies (148 mug/L) was significantly greater than in those bottle feeding (50 mug/L). This was also reflected by the finding that no breast feeding baby had a UI values < 50 mug/L in comparison to 50% of bottle feeders. The depressed values in mothers and relatively high values in their infants could present a false picture and suggest the need to defer any investigations of iodine status at this time. The findings do however suggest a need for further investigations aimed at determining the fate of iodine ingested perinatally and its possible physiological significance in maintaining thyroid status in the mother and neonate."

 

 

Dietary iodine intake in pregnancy.

Smyth PP.

Ir Med J. 2006 Apr;99(4):103.

 

"Recent publications have shown that mild maternal hypothyroidism or even asymptomatic hypothyroxinaemia can result in an intellectual deficit and/or neuropsychomotor defects and may be associated with Attention Deficit and Hyperactivity Disorder (ADHD).  In addition to iodine deficiency, children born to mothers having circulating antithyroid antibodies are at risk of impaired neurological development even if thyroid function is normal."

 

 

Iodine intake in pregnancy in Ireland--a cause for concern?

Nawoor Z, Burns R, Smith DF, Sheehan S, O'Herlihy C, Smyth PP.

Ir J Med Sci. 2006 Apr-Jun;175(2):21-4.

[abstract only]

 

"BACKGROUND: Adequate dietary iodine intake is necessary to maintain maternal thyroid function at a level permitting normal neuropsychological development of the foetus.

 

AIMS AND METHODS: To determine dietary iodine status by measuring urinary iodine excretion (UIE), proportional to dietary intake, in Irish mothers during the first trimester of pregnancy.

 

RESULTS: Median UIE showed seasonal variations, being lower in summer than in winter. The median values in pregnant women were, summer 45microg/l, winter 68microg/l. Equivalent values for controls were 43 and 91microg/l respectively. UIE required to achieve WHO recommended daily iodine intakes would be 120-180microg/l. In the Irish subjects UIE values suggestive of iodine deficiency (<50microg/l) were observed in 55% of pregnant women tested in summer and 23% in winter. Dairy milk iodine, a major dietary iodine source, showed similar variation.

 

CONCLUSIONS: While there is as yet no available evidence of widespread thyroid hypofunction in the Irish obstetric population, the findings are a cause of concern, which if confirmed by a more comprehensive investigation, may indicate the need for iodine prophylaxis."

 

 

Sequential studies on thyroid antibodies during pregnancy.

Smyth PP, Wijeyaratne CN, Kaluarachi WN, Smith DF, Premawardhana LD, Parkes AB, Jayasinghe A, de Silva DG, Lazarus JH.

Thyroid. 2005 May;15(5):474-7.

[abstract only]

 

"Thyroid antibodies were measured sequentially in 25 pregnant women from a Sri Lankan population. A high prevalence of antithyroid antibodies, particularly antithyroglobulin antibodies (TgAb) had previously been demonstrated in female schoolchildren drawn from this population. In the present study TgAb were detected in 36.8% of nonpregnant controls while thyroid peroxidase antibody (TPOAb) positivity was present in 26.3%. The prevalence of both antibodies in the pregnancy study group showed a progressive decline compared to nonpregnant controls throughout gestation becoming undetectable in the third trimester. The results are consistent with an immunosuppressive effect of pregnancy in a population in whom high thyroid autoantibody titers may have resulted from a recent salt iodization program."
 

 

Variation in iodine handling during normal pregnancy.

Smyth PP.

Thyroid. 1999 Jul;9(7):637-42.

[abstract only]

 

"Reports in the literature are divided on changes in thyroid volume and urinary iodine excretion (UI) during normal pregnancy. Reports from Ireland, an area of modest dietary iodine intake (median UI 70 microg/L) showed an increase in UI that rose to a median value of 135 microg/L in the first trimester (T1) and continued at 124 microg/L in the second (T2) and 122 microg/L in the third trimester (T3). In parallel with the increase in UI, mean ultrasound measured thyroid volume increased by a maximum of 47% over nonpregnant values in the third trimester (T3). Although these findings were consistent with studies in Cardiff, UK (median UI 73 microg/L), which also showed a pregnancy-associated rise in UI excretion (maximum 176 microg/L) accompanied by a 30% increase in median thyroid volume, they differed from findings in Sri Lanka (median UI 146 microg/L), a country in which a successful program of salt iodination has recently been implemented, which showed no significant changes in UI excretion (T3 maximum 154 microg/L) but did show a modest (20%) maximum increase in median thyroid volume at T3. Prospective studies on Irish subjects showed that median UI fell precipitously to nonpregnant control values (76 microg/L) at delivery. In addition, UI in neonates sampled at 3-days postdelivery showed that excretion was greater in breast-fed than in bottle fed infants. Differences in reported UI excretion patterns during pregnancy may reflect the existence of a threshold above which increased renal clearance results in increased iodine loss but that is masked at higher iodine intakes. Assuming constant dietary iodine intake during pregnancy, any increased urine loss will inevitably lead to negative iodine balance and thyroid depletion. In these circumstances, increased thyroid volume may in part be a compensatory mechanism to allow for greater iodine storage."
 

 

Maternal iodine status and thyroid volume during pregnancy: correlation with neonatal iodine intake.

Smyth PP, Hetherton AM, Smith DF, Radcliff M, O'Herlihy C.

J Clin Endocrinol Metab. 1997 Sep;82(9):2840-3.
 

"Differences in pregnancy-associated alterations in thyroid volume and urinary iodine (UI) excretion have been attributed to geographical variations in dietary iodine intake. In this study, ultrasound-measured thyroid volume and UI excretion were assessed during the 3 trimesters of pregnancy, at delivery, and at 6 weeks postpartum. Urine specimens also were obtained from mothers and both breast- and formula-feeding infants at 3 days after delivery. Thyroid volume showed a significant increase (maximum 47.0%), compared with nonpregnant control values over the 3 trimesters of pregnancy, which occurred as early as the first trimester and was paralleled by increased UI excretion, followed in turn by a precipitous fall at delivery. UI excretion in breast-feeding neonates (100 +/- 6.8 micrograms/L) was significantly higher than in their mothers (76 +/- 5.6 micrograms/L; p < 0.01) but was significantly lower (43 +/- 3.5 micrograms/L) in formula-fed infants. The results suggest that in an area of moderate dietary iodine intake, UI loss during pregnancy may result in maternal thyroid enlargement. The ability of the breast to transport iodine compensates for this loss in breast-fed infants, but this protection may be lost in formula feeding."

 

 

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