THYROID HORMONE PRODUCTION
Iodine is essential for the manufacture of T4 and T3, which are hormones that influence growth, maturation, thermogenesis, oxidation, myelination of the CNS and the metabolism of all tissues. The thyroid hormones, especially T3, exert their effects by binding to nuclear receptors on cell surfaces, which in turn triggers binding of the zinc fingers of the receptor protein to the DNA.
Due to the concentration of appreciable iodine levels in a range of other tissues, including salivary, gastric and lactating mammary glands, as well as the ovaries, questions remain about the potential for additional actions of iodine. One currently proposed model suggests iodine is an indirect antioxidant, via its capacity to reduce elevated TSH, a trigger of increased peroxide levels in the body.
Clinical note — Why is iodine deficiency on the rise?
The emergence or re-emergence of iodine deficiency is not limited to Australia. One study found that the median urinary iodine excretion had declined by more than 50% in between 1971 and 1994 in the United States.
Three reasons have been proposed to explain the emergence of iodine deficiency in developed countries. First, milk has traditionally been viewed as a good dietary source of iodine; however, since the 1990s its iodine content has reduced significantly because iodine-containing sanitisers have been gradually replaced with chlorine-containing sanitisers. The significance of this change within the dairy industry was recently shown by Li et al (2005) who compared the iodine content of Australian milk products from 1975 and 2004. They identified mean iodine concentrations of 593.5 µg/L and 583 µg/L from samples taken from Victoria and NSW respectively in 1975 compared to a median concentration of 195 µg/L in 2004 (250 mL providing 50-60 µg iodine). Interestingly, the same researchers demonstrated that dairy products and water in northern and central Queensland contain higher iodine levels, which may explain the lower incidence of iodine deficiency in these areas). In spite of this, a survey of dietary habits of Tasmanian schoolchildren has revealed that consumption of dairy products is associated with improved iodine status, a case of some being better than none.
A second reason may relate to public health campaigns that have resulted in increased awareness of the potential adverse effects of salt and reduced its consumption, but failed to highlight the potential benefits of a moderate intake of iodised salt. In addition, few food manufacturers use iodised salt in their products, further reducing exposure to iodine.
Lastly, the mineral depletion of soils is another possible contributing factor, in particular the depletion of selenium. Considering its role in iodine utilisation, selenium deficiency would potentiate the effects of iodine deficiency. Other theoretical considerations include increased environmental exposure to halogens, such as fluorine and chlorine, and increased consumption of goitrogens, such as soy, in the diet.
Although identifying the key factors responsible for the growth of iodine deficiency is important, many authors argue that implementation of national iodine monitoring and surveillance of the iodine content in foods is the most immediate concern. Lessons learnt from Tasmania’s iodine supplementation program, where state-wide bread fortification failed to reduce the prevalence of iodine deficiency in children, indicate that greater efforts are required to create significant improvements in iodine status.