6533b858fe1ef96bd12b64cf

RESEARCH PRODUCT

Maintenance of iodine intake

subject

description

Dietary iodine status is routinely assessed by measuring urinary iodine excretion (UI). In most European countries iodine intake is maintained at WHO recommended levels by iodisation of table salt [1]. Exceptions to this practice include Ireland and the UK where only 5% (approximately) of table salt sold is iodine supplemented. However despite the finding of relatively low median UI values in study populations in both Ireland and the UK [2-4] there is little evidence of an increased prevalence of hypothyroidism, overt or subclinical, of non autoimmune pathogenesis [5-8]. In this communication studies on iodine status in the Irish population over the years 1988-2007 are reviewed, as are investigations into how in the absence of salt iodisation, factors such as proximity to the sea or placental iodide transport/storage have a role in providing sufficient iodine to maintain euthyroid status in the study population. Subjects were not selected on a systematic basis but were a combination of available findings from different Irish populations studied over the years specified. Although most study groups were comprised of adult females, where these were not available, findings from female schoolchildren were assessed. Median values for UI in study populations ranged from approximately 50-140 µg/l. In the absence of iodised salt availability, milk and dairy products constitute a major iodine source but their content shows seasonal variation with a higher iodine content when cattle in winter housing are fed dietary supplements including iodine [9,10]. Thus UI values were lower during the summer months (April to September) and higher in Winter. The low values in Irish subjects were supported by recent findings in a study of UK female schoolchildren [4] where a median UI value of 80 µg/l corresponded to the most recent Irish value of 79 µg/l [11]. Interestingly the lowest regional value in the UK study came from Northern Ireland where Belfast children had a median UI of 62 µg/l with 30% having values 150 µg/l) were observed in 40.4% of (seaweed rich), 3.6% (lower seaweed), 2.3% (inland)) supporting the hypothesis that iodine intake in coastal regions may be influenced by seaweed abundance rather than proximity to the sea [14]. The other area of study presented is the role of the placenta in iodide transport/storage. How is iodide transported into the placenta? Is iodide transport concentration dependent? Is such transport hormone dependent? Both fresh placental tissue obtained from women undergoing elective prelabour caesarean section at term and primary cultures of trophoblastic cells accumulate radioactive 125I which could be partially blocked by perchlorate inhibition [unpublished observations]. RNA was isolated from placental trophoblasts and real time RT-PCR performed using sodium iodide symporter (NIS) and pendrin (PDS) probes. Trophoblastic cells expressed both NIS and PDS. 125I uptake in primary cultures from placental tissues was enhanced by individual pregnancy related hormones, particularly hCG and oxytocin, with synergism between hormone combinations. These incremental responses were mirrored by increased expression of NIS but not PDS when measured by Real time PCR suggesting that the increased iodide uptake was solely due to increased NIS expression. Measurement of placental tissue iodine content (mean 40ng/g tissue), while not approaching thyroid levels (~ 1,000 ng/G tissue), is significantly greater than that of other non-thyroidal tissues and appears to be directly proportional to iodine intake as determined by UI [11,15].