Iodine status of UK women of childbearing age
Authors: Bath S. , Walter A. , Taylor A. , Rayman M. 
Published: July 2008

Background:  Iodine deficiency in pregnant women can lead to impaired foetal brain development, linked to reduced intelligence quotient scores and impaired motor skills in the offspring (Haddow et al., 1999). As a result, the WHO (2007) has raised iodine requirements during pregnancy to 250 μg day−1 (compared was 150 μg day−1 for non‐pregnant adults). It is important that women meet this requirement to provide an adequate supply of thyroid hormones to the foetus. Historically, the UK was considered to have a sufficient iodine intake (Lee et al., 1994) but concern has recently been expressed about the iodine status of UK women (Kibirige et al., 2004). This study aimed to assess a cohort of UK women of childbearing age to identify the extent of any inadequacy in iodine intake.

Methods:  Twenty‐six women of childbearing age were recruited from the student and staff population of a university.Twenty‐four hour urine collections were obtained and total volumes measured. Iodide concentrations were measured using inductively coupled plasma mass spectrometry (ICP‐MS), considered the ‘gold standard’ technique (Vanderpas, 2006). Twenty‐four hour iodide excretion was calculated and used to assess the individual risk of deficiency using cut‐off values defined by Thomson et al. (1997). Iodine intake was estimated by extrapolation of 24‐h urinary iodide excretion (assuming 90% excretion rate) and this was compared to the reference Nutrient Intake (RNI) for adults and pregnant women. Ethical approval was obtained from The University Ethics Committee

Results:  The median value for urinary iodide concentration was 66 μg L−1 (IQR 42), classifying the group as mildly deficient (WHO et al., 2001). Twenty‐four iodide excretion showed that five (19%) subjects were mildly iodine deficient as urinary iodide excretion was between 50 and 100 μg in 24 h. Iodine intake (estimated from urinary iodide excretion) indicated that seven subjects (27%) did not meet the adult requirement of 150 μg day−1 and, should these subjects become pregnant, 17 subjects (65%) would not meet the 250 μg day−1 requirement.

Discussion:  The findings of this small study give cause for concern as almost a fifth of individuals were classified as mildly deficient in iodine. This could have serious consequences if these women were to become pregnant. Various limitations of the study (selection of subjects and season) suggest that this is likely to be a best‐case scenario. It may be prudent to advise pregnant women to increase their intake of iodine‐rich foods during pregnancy.

Conclusions:  This study needs to be repeated in larger and more diverse cohorts to assess the prevalence of iodine insufficiency in the UK and the subsequent risk to foetal development.

References  Haddow, J.E., Palomaki, G.E., Allan, W.C. et al. (1999) Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N. Engl. J. Med.341, 549–555.

Kibirige, M.S., Hutchison, S., Owen, C.J. & Delves, H.T. (2004) Prevalence of maternal dietary iodine insufficiency in the north east of England: implications for the fetus. Arch. Dis. Child. Fetal. Neonatal. Ed.89, 436–439.

Lee, S.M., Lewis, J., Buss, D.H. et al. (1994) Iodine in British foods and diets. Br. J. Nutr.72, 435–446.

Thomson, C.D., Colls, A.J., Conaglen, J.V., Macormack, M., Stiles, M. & Mann, J. (1997) Iodine status of New Zealand residents as assessed by urinary iodide excretion and thyroid hormones. Br. J. Nutr.78, 901–912.

Vanderpas, J. (2006) Nutritional epidemiology and thyroid hormone metabolism. Annu. Rev. Nutr.26, 293–322.

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WHO Secretariat (2007) Prevention and control of iodine deficiency in pregnant and lactating women and in children less than 2‐years‐old: conclusions and recommendations of the Technical Consultation. Public Health Nutr. 10, 1606–1611.