Year: 2013
Type: conference-abstract
Abstract: 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 < 50 µg/l. Despite the relatively low UI values obtained in the Irish study populations, findings for neonatal TSH assessed over the years 1995-2006 did not exceed 3%, a cut off point indicative of iodine deficiency. However a small but significant trend to higher TSH, within the reference range, was observed [6].
In the absence of iodine supplementation of table salt, dietary iodine intake is entirely opportunistic. Consumption of milk and dairy products obviously plays a part but this communication reports on the investigation of possible other modes of iodine intake aimed at establishing if living near the sea in a seaweed abundant environment, and therefore exposed to gaseous I2 ingestion by respiration, may confer advantages in terms of iodine intake. Also, as adequate iodine nutrition for the foetus depends not only on maternal iodine supply, but also on the ability of the placenta to successfully transport iodide to the foetal thyroid for use in thyroid hormone biosynthesis, it is proposed to report on placental uptake and possible storage of iodine as a means of maintaining adequate iodine intake in utero.
Ireland has traditionally been regarded as an area of borderline iodine deficiency which might not be expected on an island where few live more than 200Km from the sea. However as has become apparent in recent times, availability of iodine in the diet is dependent on many factors, of which consumption of seafoods is but one. Seaweed is the major source of iodine and for this study we utilised for iodine intake studies measurements whose purpose was to determine the concentration of gaseous I2 released by seaweeds and its effect on cloud formation and changes in weather [12,13]. To determine a possible role for seaweed derived atmospheric iodine ingestion in human populations, urine samples were obtained from female schoolchildren and adults living in coastal areas seaweed rich and of low seaweed abundance and in inland areas of Ireland. Atmospheric I2 was greatest over the seaweed mass but crude calculations based on a daily inspiration of 10,000 L of air could only provide a potential increment of ~30 µg/day additional iodine [14]. Most would receive considerably less. Despite this relatively low potential I2 intake, UI in populations living near a seaweed hotspot were much higher than in lower abundance seaweed coastal or inland areas (158, 71 and 58 µg/l, respectively). Higher 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].
Source: Thyroid Research
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $2,790
OpenAlex ID: W2055910943