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Iodine status of women of childbearing age in Scotland

Published online by Cambridge University Press:  19 October 2012

M. Lampropoulou ,
M. E. J. Lean  and
E. Combet
M. Lampropoulou
Affiliation:
Human Nutrition, School of Medicine, University of Glasgow, Yorkhill Hospital, Dalnair Street, Glasgow, G3 8SJ, UK
M. E. J. Lean
Affiliation:
Human Nutrition, School of Medicine, University of Glasgow, Yorkhill Hospital, Dalnair Street, Glasgow, G3 8SJ, UK
E. Combet
Affiliation:
Human Nutrition, School of Medicine, University of Glasgow, Yorkhill Hospital, Dalnair Street, Glasgow, G3 8SJ, UK
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Abstract

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Information
Proceedings of the Nutrition Society , Volume 71 , Issue OCE2: Summer Meeting hosted by the Irish Section, 16–19 July 2012, Translational nutrition: integrating research, practice and policy , 2012 , E143
Copyright
Copyright © The Authors 2012

Iodine deficiency is one of the three key micronutrient deficiencies highlighted as a major public health issue by the World Health Organisation (WHO) and it represents a particular challenge for pregnant women and young children. Indeed, iodine is required for the synthesis of thyroid hormones, which are critical for normal neurodevelopment of the infant. Thus, iodine deficiency has been coined “the most common cause of preventable mental impairment worldwide”( Reference Zimmermann, Jooste and Pandav 1 ). With recent evidence that most UK school-girls are iodine deficient( Reference Vanderpump, Lazarus and Smyth 2 ), this study aimed to assess iodine status of women of childbearing age in Scotland, along with habitual intake of iodine-rich foods.

Women (n=381, aged 18–44, median age 30 years, sd 8) were recruited in the West of Scotland from July 2010 to August 2011. A casual spot urine sample was collected, and urinary iodine (UI) was analysed using persulfate digestion followed by Sandel-Kolthoff colorimetric reaction( Reference Ohashi, Yamaki and Pandav 3 ). Iodine status was classified according to the WHO cut-offs, with mild iodine deficiency defined as UI<100 μg/l, moderate deficiency as UI<50 μg/l, and severe deficiency as UI<20 μg/l( 4 ). Socio-demographic data was collected, and iodine-rich foods consumption was measured using a food frequency questionnaire based on a modified version of an existing questionnaire( Reference Lean, Anderson and Morrison 5 ).

The median urinary iodine was 75 μg/l, indicative of mild iodine deficiency; 64% of the samples had a urinary iodine concentration below 100 μg/l while 31% of the samples had a urinary iodine concentration below 50 μg/l. Deprivation (SIMD) quintiles were equally represented among the sample. There was no significant difference in urinary iodine concentration between deprivation quintiles, ethnicity, education and income categories, or age categories (18–26 y, 27–35 y and 36–44 y). Multivariate linear regression revealed a strong correlation between urinary iodine and milk intake (rs =0.15, p<0.004), but not fish intake.

Our results are consistent with data obtained recently UK-wide for girls aged 14–15( Reference Vanderpump, Lazarus and Smyth 2 ). According to the WHO, no more than 20% of a population should have urinary iodine values below 50 μg/l( 4 ), but sour sample exceeds this threshold. The absence of iodine prophylaxis in the UK makes women of childbearing age and their future offspring a vulnerable group. With iodine requirement increasing from 140 to 250 μg per day during pregnancy, it is essential that women of childbearing age are provided with sufficient information to make dietary choices ensuring adequate amounts of iodine to cover their needs.

References

1. Zimmermann, M, Jooste, P & Pandav, C (2008) Lancet 372, 1251–1262.CrossRefGoogle Scholar
2. Vanderpump, M, Lazarus, J, Smyth, P et al. (2011) Lancet 377, 2007–2012.CrossRefGoogle Scholar
3. Ohashi, T, Yamaki, M, Pandav, CS et al. (2000) Clin Chem 46, 529–36.CrossRefGoogle Scholar
4. World Health Organization. United Nations Children's Fund & International Council for the Control of Iodine Deficiency Disorders. Assessment of iodine deficiency disorders and monitoring their elimination. 3rd ed. Geneva, Switzerland: WHO, 2007.Google Scholar
5. Lean, MEJ, Anderson, AS, Morrison, C et al. (2003) Eur J Clin Nutr 57, 667–673.CrossRefGoogle Scholar