Iodine

Background

Iodine was one of the first trace elements to be identified as essential. In the 1920s it was shown to be an integral component of the thyroid hormone, thyroxine (T4), required for normal growth and metabolism. Soon after, it was recognised as a component of 3,5,3'-tri-iodothyronine (T3), a key regulator of important cell processes. The thyroid hormones are required for normal growth and development of tissues such as the central nervous system and have a broader role in maturation of the body as a whole. They are important for energy production and oxygen consumption in cells thereby helping to maintain the body's metabolic rate. Iodine occurs in tissues in both organic and organically bound forms. The iodine content of the adult body is approximately 15-20 mg, of which 70-80% is in the thyroid gland - which concentrates iodine (Freake 2000) - and the rest is in blood.

Once iodine is absorbed in the form of iodide and reaches the circulation, it is concentrated in the thyroid gland where it is converted to iodine and combined with tyrosine residues of thyroglobulin. The iodinated tyrosines are removed from the thyroglobulin by proteolytic enzymes and T4 is released into the circulation (Kidd et al 1974). T4 is inert until deiodinated either to T3 (or reverse T3, an inactive form of T4). Deiodination requires selenocysteine as the active form of selenium in the iodothyronine deiodinases (Arthur & Beckett 1999). Regulation of thyroid hormone synthesis, release and action is complex. It involves the thyroid, pituitary, brain and peripheral tissues. Excess inorganic iodine is readily excreted in urine, with smaller amounts in faeces and sweat (Lamberg 1993).

Iodine in foods is in the inorganic iodide form and is easily absorbed in the stomach and upper small intestine (Sumar & Ismail 1997) as is supplemental iodine. Thus the amount of bioavailable iodine depends on the amount consumed rather than the chemical form or composition of the diet (Fairweather-Tait & Hurrell 1996). However, the utilisation of absorbed iodine is influenced by goitrogens. Goitrogens such as sulphur-containing thionamides found in brassica vegetables such as cabbage, broccoli and brussel sprouts can interfere with the synthesis of the thyroid hormones. They impair the binding of iodine to thyroglobulin and prevent oxidation of iodide by thyroid iodide peroxidase (Gaitan 1980). Foods containing goitrogenic cyanoglucosides such as sweet potato and maize release thiocyanate that competes with iodide, blocking its uptake by the thyroid (Gaitan 1980, Lamberg 1993).

The iodine content of most foods is low and can be affected by soil, irrigation and fertilisers. Losses can occur in cooking. Most soils in New Zealand are low in iodine resulting in low concentrations in locally grown foods. The major food sources are of marine origin. Processing aids such as calcium iodate, potassium iodate, potassium iodide and cuprous iodide act to increase the content of iodine in certain foods. Iodophores used by the dairy industry, which opportunistically enter the food supply, were the major, if not the prime, contributors to intake of iodine in Australia and New Zealand in the 1960s. However, controls introduced in the early 1970s saw changes in practices leading to reduced iodine in milk. As the use of iodised salt has also declined since that time, intakes of iodine have fallen in both Australia and New Zealand (Eastman 1999, Gunton et al 1999, Hynes et al 2004, Skeaff et al 2002, 2005, Thomson 2002, 2004).

Iodine deficiency results in a range of conditions collectively termed 'iodine deficiency disorders' (Hetzel et al 1990, Thomson 2002). In severe deficiency, these include major effects on the foetus, such as abortion or stillbirth, congenital anomalies, increased perinatal and infant mortality, neurological cretinism or mental deficiency with deaf mutism, spastic diplegia and squint, myxoedematous cretinism and dwarfism and psychomotor effects. In neonatal life, childhood or adulthood, iodine deficiency can lead to goitre or hypothyroidism as well as impaired mental and physical development.

Several indicators are used to assess iodine requirements, including urinary iodide excretion, thyroid hormones in plasma or serum, assessment of thyroid size and goitre rate, radioactive iodine uptake, balance studies and epidemiologic, population studies. Thyroid iodine accumulation and turnover is generally considered to be the best measure.

1 mmol iodine = 127 mg iodine

Recommendations by life stage and gender

Infants

Age AI
0-6 months 90 µg/day
7-12 months 110 µg/day

Rationale: The AI for 0-6 months was calculated by multiplying the average intake of breast milk (0.78 L/day) by the average concentration of iodine in breast milk (115 µg/L), and rounding. The figure used for breast milk was that recommended by FAO:WHO (2001) which is also consistent with the study of Johnson et al (1990) in New Zealand. The AI for 7-12 months was extrapolated from that of younger infants using a metabolic weight ratio.

Children & adolescents

Age EAR RDI
All
1-3 yr 65 µg/day 90 µg/day
4-8 yr 65 µg/day 90 µg/day
Boys
9-13 yr 75 µg/day 120 µg/day
14-18 yr 95 µg/day 150 µg/day
Girls
9-13 yr 75 µg/day 120 µg/day
14-18 yr 95 µg/day 150 µg/day

Rationale: The EAR for children was based on balance studies for the age groups 1-3 years, 4-8 years and 14-18 years (Ingenbleek & Malvaux 1974, Malvaux et a 1969) and by extrapolation from adults using metabolic body weight ratios for 9-13 year olds. The RDI was set assuming a CV of 20% for the EAR from studies in adults (FNB:IOM 2001), and rounded.

Adults

Age EAR RDI
Men
19-30 yr 100 µg/day 150 µg/day
31-50 yr 100 µg/day 150 µg/day
51-70 yr 100 µg/day 150 µg/day
>70 yr 100 µg/day 150 µg/day
Women
19-30 yr 100 µg/day 150 µg/day
31-50 yr 100 µg/day 150 µg/day
51-70 yr 100 µg/day 150 µg/day
>70 yr 100 µg/day 150 µg/day

Rationale: The EARs for adults were based on iodine balance studies indicating that iodine balance is achieved at intakes over 100 µg/day but not below 40 µg/day. From these data, particularly the iodine accumulation and turnover studies, and a New Zealand study in adults relating urinary iodide to thyroid volume (Thomson et al 2001) that indicated physiological requirements of 85-100 µg/day, a value of 100 µg/day was adopted for the EAR. The RDI was set assuming a CV of 20% for the EAR (FNB:IOM 2001), and rounded up to reflect the possible influence of natural goitrogens.

Pregnancy

Age EAR RDI
14-18 yr 160 µg/day 220 µg/day
19-30 yr 160 µg/day 220 µg/day
31-50 yr 160 µg/day 220 µg/day

Lactation

Rationale: The EAR for pregnancy was based on data relating to the thyroid content of newborns, iodine balance studies and iodine supplementation studies in pregnancy (FNB:IOM 2001). The RDI was set assuming a CV of 20% for the EAR.

Age EAR RDI
14-18 yr 190 µg/day 270 µg/day
19-30 yr 190 µg/day 270 µg/day
31-50 yr 190 µg/day 270 µg/day

Rationale: The EAR for lactation was based on the adult female needs (100 µg/day) and the replacement needs for iodine secreted in breast milk (90 µg/day). The RDI was set assuming a CV of 20% for the EAR.

Upper Level of Intake

Age UL
Infants
0-12 months Not possible to establish. Source of intake should be milk, formula and food only
Children and adolescents
1-3 yr 200 µg/day
4-8 yr 300 µg/day
9-13 yr 600 µg/day
14-18 yr 900 µg/day
Adults 19+ yr
Men 1,100 µg/day
Women 1,100 µg/day
Pregnancy
14-18 yr 900 µg/day
19-50 yr 1,100 µg/day
Lactation
14-18 yr 900 µg/day
19-50 yr 1,100 µg/day

Rationale: The first effect seen in iodine excess is challenged thyroid function by elevated TSH concentrations. This is the critical adverse effect (FNB:IOM 2001). Two studies of TSH concentrations after supplemental iodine showed increased TSH at 1,800 µg/day and 1,700 µg/day (Gardner et al 1988, Paul et al 1988) indicating a LOAEL of 1,700 µg/day. A UF of 1.5 is applied to derive a NOAEL that is the basis of the UL for adults. As there is little evidence for other age groups, ULs for children and adolescents were extrapolated from the adult recommendation on a metabolic body weight basis. The adult UL was also used for pregnancy and lactation as there was no evidence of increased sensitivity associated with these.

Note: Individuals with thyroid disorders or a long history of iodine deficiency may still respond adversely at levels of intake below the UL.

References

Arthur JR, Beckett GJ. Thyroid function. Br Med Bull 1999;55:658-68.

Eastman CJ. Where has all the iodine gone? Med J Aust 1999;171:455-6.

Fairweather-Tait S, Hurrell RF. Bioavailability of minerals and trace elements. Nutr Res Revs 1996;9:295-324.

Food and Agricultural Organization: World Health Organization. Human vitamin and mineral requirements. Report of a joint FAO:WHO expert consultation. Bangkok, Thailand. Rome: FAO, 2001.

Food and Nutrition Board: Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, manganese, Molybdenum, Nickel, Silicon, Vanadium and Zinc. Washington DC: National Academy Press, 2001.

Freake HC, Iodine. In: Stipaunk M, ed. Biochemical and physiological aspects of human nutrition. Philadelphia: W.B. Saunders Company, 2000.

Gaitan E. Goitrogens in the etiology of endemic goiter. In: Stanbury JB, Hetzel BS, eds. Endemic goiter and endemic cretinism. New York: Wiley Medical, 1980.

Gardner DF, Centor RM, Tiger RD. Effects of low dose oral iodine supplementation on thyroid function in normal men. Clin Endocrinol 1988;28:283-8.

Gunton JE, Hams G, Fiegert M, McElduff A. Iodine deficiency in ambulatory patients at a Sydney teaching hospital: is Australia truly iodine replete? Med J Aust 1999;171:
467-70.

Hetzel BS, Potter BJ, Dulberg EM. The iodine deficiency disorders: nature, pathogenesis and epidemiology. World Rev Nutr Diet 1990;62:59-119.

Hynes KL, Blizzard CL, Venn AJ, Dwyer T, Burgess J. Persistent iodine deficiency in a cohort of Tasmanian school children: associations with socio-economic status, geographic location and dietary factors. Aus NZ J Public Health 2004;28:476-81.

Ingenbleek Y, Malvaux P. Iodine balance studies in protein-calorie malnutrition. Arch Dis Child 1974;49:305-9.

Johnson LA, Ford HC, Doran JM, Richardson VF. A survey of the iodide concentration of human milk. NZ Med J 1990;103:393-4.

Kidd PS, Trowbridge GL, Goldsby JB, Nichan MZ. Sources of dietary iodine. J Am Diet Assoc 1974;65:420-2.

Lamberg B. Iodine deficiency disorders and goitre. Eur J Clin Nutr 1993;47:1-8.

Malvaux P, Becckers C, de Visscher M. Iodine balance studies in nongoitrous children and in adolescents on low iodine intake. J Clin Endocrinol Metab 1969;29:79-84.

Paul T, Meyers B, Witorsch RJ, Pino S, Chipkin S, Inbar SH, Braverman LE. The effect of small increases in dietary iodine on thyroid function in euthyroid subjects. Metab 1988;37:121-4.

Skeaff SA, Thomson CD, Gibson RS. Mild iodine deficiency in a sample of New Zealand schoolchildren. Eur J Clin Nutr 2002;56:1169-75.

Skeaff S, Ferguson E, Valeix P, Gibson R, Thomson CD. Are breast-fed infants and toddlers in New Zealand at risk of iodine deficiency? Nutrition 2005;21:325-31.

Sumar S, Ismail H. Iodine in food and health. Nutr Food Sci 1997;5:177-83.

Thomson CD. Selenium and iodine intakes and status in New Zealand and Australia. Br J Nutr 2004;91:661-72.

Thomson CD, Packer MA, Butler JA, Duffield AJ, O'Donaghue KL, Whanger PD. Urinary selenium and iodine during pregnancy and lactation. J Trace Elements Med Biol 2001;14:210-7.

Thomson CD. Australian and New Zealand Nutrient Reference Values for Iodine. Technical Report to Ministry of Health. Dunedin: University of Otago, 2002.