Iodine deficiency disorders (IDDs) present throughout the life cycle (Table 1) and represent a major cause of morbidity on a global scale. As recently as 12 years ago, the World Health Organization (WHO) estimated that 1.6 billion people worldwide were at risk of iodine deficiency. The most damaging effect of a deficiency of this trace element is on the developing brain, and at least 20 million were believed to be suffering from impaired mental function. Thus, iodine deficiency is the world’s greatest single cause of preventable brain damage and mental retardation. The detrimental effects on mental performance can have profound social consequences and influence national development. Even in the absence of cretinism, iodine deficiency adversely affects growth and development – physical as well as neuropsychological. Goitre, first described and treated with seaweed and other marine products several thousand years BC in China, is the most obvious of the IDDs, and occurs at lesser degrees of iodine deficiency.

The iodine content of plant and animal foods reflects the iodine content of the soil, which is typically deficient in parts of the world where iodine has been leached from the soil by high rainfall or glaciation. In these areas, clinical deficiency is especially prevalent when groups or populations exist largely or exclusively on locally sourced foods and have a low intake of marine foods, which are a rich source of iodine. Goitre is typically seen when intake is less than 50 μg iodine/day and cretinism with intakes by the mother of 30 μg or less per day. Usual intakes range between 80–150 μg/day, though some countries (eg, Canada and Japan) have appreciably higher intakes. New Zealand has a very low level of iodine in the soil in many areas, so not surprisingly goitre was endemic in many parts of the country. In the early years of the last century, surveys suggested that about one third of school children may have had significant thyroid enlargement, with an approximately comparable number having some increase in size of the gland.2 Iodisation of salt, first implemented in Switzerland in 1920, was introduced in New Zealand in 1924. At first, introduction concentration was too low and little was achieved. However, the concentration was increased in 1938 and remains at a similar level today. This is believed to have contributed to the dramatic reductions in goitre rates. In 1953, surveys of school children suggested that rates had fallen to about 1%. This observation, together with the results of further surveys showing improved iodine status in the 1960s and 1980s, led to reduced attention to iodine deficiency as a health issue in this country.3–5 Iodised oil by injection, iodine supplements, and iodisation of bread, drinking water, sugar and animal feeds are methods that have also been used successfully in some countries to improve iodine intake.

Interest in iodine deficiency as a possible public health issue was rekindled in 1997 by the publication of a survey of adult blood donors in Dunedin and the Waikato carried out during 1993 and 1994.6 Iodine status is typically assessed by determining 24-hour urinary iodide excretion, based on the assumption that approximately 90% of iodine intake is excreted in the urine. Information regarding iodine status can be supplemented by measurement of circulating thyroid hormones and thyroid stimulating hormone (an especially useful indicator in neonates), and assessment of goitre rates using simple clinical criteria or thyroid volume by ultrasonography. When excluding subjects taking dietary supplements including iodine, median urinary iodide excretion was 70 μg/day for men and 59 μg/day for women, implying an intake perilously close to the suggested ‘critical low intake’ (CLI) for adult men and women, 60 μg/day.7 The CLI is defined as that level below which virtually all people would be at high risk of having an inadequate intake. Below an intake of about 50 μg/day, absolute uptake of iodide falls, the iodine content of the thyroid decreases and risk of goitre increases appreciably. In a later study in Otago adults,8 although blood concentration of thyroid hormones was normal, when subjects were grouped according to urinary iodine, the low iodine group (46 ± 9 μg/day) had a higher mean thyroid volume than the medium (74 ± 8 μg/day) and high (136 ± 54 μg/day) groups. This suggests that a mean excretion of around 75 μg/day, representing an intake of at least 85 μg/day, is necessary to prevent the consequences of an inadequate iodine intake. Furthermore, using the World Health Organization estimate for iodine deficiency disorders, 5% were at severe risk (median urinary iodide excretion <20 μg/l), 26% were at moderate risk (median excretion 20–49 μg/l), and half were at mild risk (median excretion 50–90 μg/1) of IDD.

Arguably of greater concern were the findings of Skeaff, Thomson and Gibson,9 published at the end of 2002, relating the iodine status of three hundred 8 to10-year-old school children in Dunedin and Wellington taken in 1996 and 1997. In this study, 3.6% (95% CI: 1.1–6.2) of the children had urinary iodine levels less than 20 μg/l; 31.4% (95% CI: 24.2–38.6) less than 50 μg/l; and 80% (95% CI: 74.1–85.3) less than 100 μg/l, representing severe, moderate and mild IDD respectively. An incidence of goitre greater than 5% is considered endemic, and Skeaff et al found that 11.3% of the children had thyroid volumes greater than the upper limit of normal using 2001 WHO cut-offs by age. Although 83% reported that iodised salt was used in the home, about one third of the children’s caregivers did not use iodised salt in cooking and about half of the children did not use iodised salt at the table. Milk and dairy products were the only potentially good sources of dietary iodine consumed daily, though most consumed red meat, chicken and eggs at least weekly. The New Zealand Children’s Nutrition Survey, currently underway, is based on a representative national sample and should help to confirm or refute these findings, but it is noteworthy that successive New Zealand Total Diet Surveys between 1987 and 1998, using modelled (or simulated) diets, have suggested a reduction in iodine intakes in adults and in children.10 It is important, therefore, to consider possible explanations for the change in intakes, potential clinical relevance, and appropriate public health measures.

Three plausible reasons have been offered to explain a reduction in intakes. First, there has been a decline in the use of iodophors as sanitisers in the dairy industry over the past two decades.11,12 It is quite conceivable that this ‘contaminant’ of milking equipment provided a significant source of iodine through intake of milk and dairy products. The use of alternative sanitisers has resulted in reduced intake from this source. A second reason is that people may indeed have heeded the public health advice to reduce discretionary intake of salt, with a concomitant reduction in iodine. However, the findings of Skeaff et al,9 that iodised salt was not always used in home cooking and at the table, also suggest an element of complacency with regard to the importance of iodine in the New Zealand diet. The third possible factor is that there are more meals eaten away from the home and pre-prepared foods purchased (ie, less food prepared in the home) and salt used in manufacturing is usually non-iodised. The fact that the most obvious clinical consequences of iodine deficiency had all but disappeared may well have led to consumers not ensuring that discretionary salt was always iodised.

The clinical consequences of mild iodine deficiency are uncertain. There is no doubt that measurable functional changes in iodine metabolism occur and risk of goitre increases as average population intakes move downwards towards the CLI; indeed this observation forms the justification for the level set. Even though there is no clear evidence of impaired intellectual function or growth retardation at marginal levels of intake, these observations together with the apparent reduction in intakes warrants some action. This is especially so if the decreasing levels of intake are confirmed by the Children’s Nutrition Survey, the first truly national survey of iodine status to be undertaken in New Zealand.

What action should be considered? Iodine supplements are not a good idea as a public health measure. The safe upper limit of intake has been set by various authorities as between 1000 and 2000 μg daily. While adverse effects of a high intake are unlikely when the thyroid gland is healthy, those who habitually have a low intake as well as those with abnormalities of the thyroid gland may respond adversely. People over the age of 40 years with multinodular goitre are at particular risk of iodine-induced hyperthyroidism. Consumption of seaweed and other iodine-containing dietary supplements, such as kelp tablets, may lead to intake beyond the safe upper limit and are therefore not recommended for use in New Zealand. The first and immediate approach is probably to remind health professionals and the public of the importance of this trace element in the human diet and that there is increasing evidence for re-occurrence of iodine deficiency in New Zealand. Milk and low-fat dairy products have traditionally been regarded as good sources and remain important, but with the reduction in use of iodophors, are not as good a source as they used to be. Eggs, fish and shellfish are good sources of iodine. Foods containing seaweed, such as sushi, are finding their way into the diet of many New Zealanders and are of course excellent dietary sources, even though concentrated seaweed supplements are not recommended. Advice to limit the discretionary intake of salt continues to be an important component of dietary guidelines, and concern over low intakes of iodine should not influence such advice. However, the benefits of always purchasing and using iodised salt for home use should be emphasised. The joint Australia New Zealand Food Standards Code contains Standard 2.10.2 Salt and Salt Products, which includes the composition of iodised salt and iodised reduced sodium mixtures, as shown in Table 2.

In the future, consideration will need to be given to the possibility of mandatory iodisation of one or more staple foods. Of no help to the public health of New Zealanders is the widespread promotion of non-iodised forms of salt by key people such as chefs, in particular those presenting cooking programmes to the nation on television. Where salt is used in food preparation or added to food it should always be iodised salt.

Continued monitoring of the iodine status of the food supply and population is imperative. It is encouraging that work is being undertaken in New Zealand with the commencement of the joint Australia New Zealand review of nutrient reference values, as well as a joint Ministry of Health and New Zealand Food Safety Authority project to address the re-emergence of iodine deficiency in New Zealand. As any change in the fortification of foods with iodine is now managed by Food Standards Australia New Zealand (FSANZ), this issue will be the first significant public health intervention in New Zealand for this agency to manage.

Author information: Jim I Mann, Professor in Human Nutrition and Medicine, Department of Human Nutrition, University of Otago, Dunedin; Elizabeth Aitken, Senior Advisor (Nutrition), Ministry of Health

Correspondence: Professor J Mann, Department of Human Nutrition, University of Otago, P O Box 56, Dunedin. Fax: (03) 479 7959; email: jim.mann@stonebow.otago.ac.nz