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Editorial

Where has all our iodine gone?

The possible re-emergence of iodine deficiency in Australia needs to be investigated in national surveys

MJA 1999; 171: 455-456

Most countries in the world, including Australia, are signatories to the United Nations-sponsored "Declaration for the Survival, Protection and Development of Children", which states that "every child has the right to an adequate supply of iodine to ensure its normal development".1 One teaspoon of iodine is all a person requires in a lifetime, yet iodine deficiency at critical stages of development in fetal life and early childhood remains the world's single most important and preventable cause of mental retardation.2

For the past three to four decades iodine deficiency has not been of significant concern in Australia (except in Tasmania); it was considered largely a problem of developing countries. That is what we thought until Gunton and colleagues give us a wake-up call with their article in this issue of the Journal 3. They found evidence of mild to moderate iodine deficiency in pregnant women, patients with diabetes and a small group of volunteers attending a Sydney teaching hospital. In their study, median urinary iodine concentrations ranged from 64 µg/L in the volunteers to 104 µg/L in pregnant women. The World Health Organization's standard for iodine-deficiency disorders in population surveys recommends that a median urinary iodine concentration above 100 µg/L is evidence against significant iodine deficiency in that population.4 Other population indicators of iodine deficiency, including total goitre rates in school-age children and serum thyrotropin (TSH) levels in the newborn, were not assessed in the Sydney study. The data of Gunton and colleagues indicate that the pregnant women they tested are ingesting less than half the recommended iodine intake in pregnancy of 200 µg/day. Although this study was not a national survey, and the sample size was small, the findings are alarming and raise concern that a major public health problem may be developing in the Australian community which could put future generations at risk of iodine-deficiency disorders.

The key factor in the genesis of iodine-deficiency disorders is decreased production of thyroxine from the thyroid gland. While endemic goitre is the most easily recognised and best-known consequence of iodine deficiency, it is probably the least important. At critical periods in fetal development and in early childhood, biochemical hypothyroidism, due to iodine deficiency, results in a wide range of devastating and irreversible effects now known as iodine-deficiency disorders.5 More recently, we have come to appreciate that there is a general diminution in intelligence in iodine-deficient communities such that iodine deficiency is considered to be the commonest cause of preventable intellectual disability worldwide.2 Further, there is now very good evidence that a small decrease in serum free thyroxine level during pregnancy, either because of iodine deficiency or thyroid disease, is an important risk factor for impaired psychomotor development in infants.6,7 The recent demonstration of intellectual impairment in the children of American women who had mild hypothyroidism in pregnancy highlights the need for better detection and treatment of hypothyroidism in early pregnancy, irrespective of its cause.8

Tasmania is the only Australian State where regular surveillance of iodine nutrition is undertaken and records are maintained. Other data are available from the Australian Centre for Control of Iodine Deficiency Disorders (ACCIDD), located at Westmead Hospital, which has performed sporadic surveys of urinary iodine excretion levels in small samples of Australians for the past two decades. In 1992 we reported that the mean urinary iodine excretion level in Sydney residents was 180 µg/L, and over 200 µg/L in Tasmanian children.9 Since then, our sporadic surveys have shown a gradual but sustained decline in urinary iodine excretion levels in Sydney residents. We recently found similar results to those of Gunton et al 3 in a survey of primary schoolchildren from western Sydney who had a median urinary iodine concentration of 84 µg/L, and in 16% of whom the iodine concentration was less than 100 µg/L. Further, unpublished results we obtained in healthy pregnant women were also very similar to those of Gunton et al, indicating that widespread mild iodine deficiency threatens to affect the most vulnerable in our community.

Why is our iodine intake decreasing in Australia? Gunton and colleagues implicate a combination of factors. Firstly, for over three decades, we have been dependent on iodine in milk contaminated by cleaning solutions used in the dairy industry; these solutions are gradually being replaced by others which leave less iodine in milk. Secondly, we seem to be using less iodised salt, through a combination of purchasing uniodised salt for domestic consumption, probably decreasing our salt consumption, and consuming most of our salt in processed foods, which, as far as we can ascertain, is uniodised. The problem is not unique to Australia, as similar downward trends in iodine intake have recently been noted in other developed countries such as the United States10 and New Zealand.11

What actions should be taken in response to these findings? Firstly, we need more information through a national survey of urinary iodine excretion and goitre rates to determine the status of iodine nutrition throughout Australia. Secondly, we need to educate the population and healthcare providers about the insidious and harmful effects of iodine deficiency, especially during pregnancy and early childhood. Finally, we must institute effective and sustainable means of iodine supplementation to our whole community through legislating for universal salt iodisation, so that all salt used for human and animal consumption in Australia is iodised. Iodising all edible salt will cost less than 10 cents per person annually. In the past this intervention has been viewed as politically unacceptable, but the debate was conducted with a view to eliminating endemic goitre without any real understanding of the often subtle, but devastating, consequences of impaired brain development. In the interim, every effort should be made to ensure every pregnant woman ingests an adequate amount of iodine to ensure her unborn child experiences normal mental development. Until we have educated the population as a whole about the risks of iodine deficiency and instituted mandatory iodisation of all salt for human and animal consumption, it may be prudent to recommend supplementary iodine for all pregnant women from the time of conception until weaning of the infant.

Creswell J Eastman, AM
Director, Institute of Clinical Pathology and Medical Research
Westmead Hospital, Westmead, and Clinical Professor of Medicine
University of Sydney, Sydney, NSW

  1. World Declaration on the survival, protection and development of children and a plan of action for implementing the world declaration on the survival, protection and development of children in the 1990s. New York: United Nations, 1990.
  2. World Health Organization. Progress towards the elimination of Iodine Deficiency Disorders (IDD). WHO/NHD/99.4. Geneva: WHO, 1999.
  3. Gunton JE, Hams G, Fiegert M, McElduff A. Iodine deficiency in ambulatory patients attending a Sydney teaching hospital: Is Australia truly iodine replete? Med J Aust 1999; 171: 467-470.
  4. World Health Organization. WHO, UNICEF, ICCIDD. Indicators for assessing iodine deficiency disorders and their control through salt iodisation. WHO/NUT/94.6. Geneva: WHO, 1994.
  5. Boyages SC. Clinical Review 49, Iodine deficiency disorders. J Clin Endocrinol Metab 1993; 77: 587-591.
  6. Pop VJ, Kuijpens JL, van Baar AL, et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol 1999; 50: 149-155.
  7. Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neurological development of the child. N Engl J Med 1999; 341: 549-555.
  8. Utiger RD. Maternal hypothyroidism and fetal development. N Engl J Med 1999; 341: 601-602.
  9. Eastman CJ. The status of iodine nutrition in Australia. In: Delange F, Dunn JT, Glinoer D, editors. Iodine deficiency in Europe -- a continuing concern. New York: Plenum Press, 1993: 133-139.
  10. Dunn JT. What's happening to our iodine? [editorial]. J Clin Endocrinol Metab 1998; 83: 3398-3400.
  11. Thomson CD, Colls AJ, Conaglen JV, et al. Iodine status of New Zealand residents as assessed by urinary iodide excretion and thyroid hormones. Br J Nutrition 1997; 78: 901-912.

©MJA 1999
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