Minerals and Trace Elements 225to iodine-replete individuals, those with IDDs or pre-
viously exposed to iodine-defi cient diets may react to
sudden moderate increases in iodine intake, such
as from iodized salt. Iodine-induced thyrotoxicosis
(hyperthyroidism) and toxic nodular goiter may
result from excess iodine exposure in these indivi-
duals. Hyperthyroidism is largely confi ned to those
over 40 years of age and symptoms are rapid heart
rate, trembling, excessive sweating, lack of sleep, and
loss of weight and strength.
Individuals who are sensitive to iodine, usually
have mild skin symptoms, but very rarely fever, sali-
vary gland enlargement, visual problems, and skin
problems, and, in severe cases, cardiovascular col-
lapse, convulsions, and death may occur. The occur-
rence of allergic symptoms, for example to iodine
medications or antiseptics, however, is rare.
Genetic diseases
Pendred’s syndrome is an autosomal recessive inher-
ited disorder with a frequency of 100 or less per
100 000. It is characterized by goiter and profound
deafness in childhood and is caused by mutations in
the Pendrin gene located on chromosome 7. The gene
codes for pendrin, a transporter protein for chloride/
iodine transport across the thyroid apical membrane.
This results in defective iodination of thyroglobulin.
Mutations in another gene, the sodium/iodide sym-
porter (NIS) gene, occasionally cause defective iodide
transport and goiter, whereas single nucleotide poly-
morphisms in the TSH receptor gene may predispose
individuals to the hyperthyroidism of toxic multi-
nodular goiter and Graves’ disease.
Assessing status
The critical importance of iodine for the thyroid
indicates that iodine status is assessed by thyroid
function. A standard set of indicators (goiter by
palpation, thyroid volume by ultrasound, median
urinary iodine, and whole blood TSH) is used to
determine prevalence in countries with endemic
defi ciency. Measurement of plasma thyroid hormones
(TSH, T 4 , and T 3 ) provides useful indicators of func-
tional iodine status in the individual. Of these, TSH
is the most sensitive functional indicator of subopti-
mal iodine status. Concentrations of T 4 decline in
more severe iodine defi ciency whereas T 3 concentra-
tions decline only in the most severe of iodine
defi ciencies.
Dietary intakes and requirements
Requirements in infancy and childhood range from
40 to 150 μg iodine/day. Adult requirements are esti-
mated at 150 μg iodine/day, increasing to 175 and
200 μg/day for pregnancy and lactation. The UL for
adults is set at 600 μg/day (EU) and at 1.1 mg/day
(USA).
Under normal circumstances, about 90% of iodine
intake is from food, with about 10% from water. The
concentration of iodine in most foods is low and, in
general, refl ects the iodine content of the soil, water,
and fertilizers used in plant and animal production.
In most countries other sources, such as iodized salts
or foods, are required. Seafoods and seaweed concen-
trate iodine from seawater and are particularly rich
sources. In some populations, milk has become a
major source of iodine, owing to the use of iodized
salt licks and iodine-enriched cattle feed for dairy
herds. Minor amounts may come from adventitious
contamination from iodophor disinfectants (teat-
dip). Iodine-enriched cattle feed will also increase the
iodine content of meat for beef herds raised on con-
centrated feedstuffs. Processed foods contribute some
additional iodine from food additives, such as calcium
iodate used in the baking industry.Micronutrient interactions
From a public health viewpoint, the most important
metabolic interaction of iodine with other micronu-
trients is with selenium. Adequate selenium status is
essential for thyroid hormone metabolism and, there-
fore, normal growth development, by ensuring suffi -
cient T 3 supply to extrathyroidal tissues. Most T 3 is
formed from T 4 by the selenium-dependent de-
iodinases. Iodine and selenium defi ciencies overlap in
various parts of the world and concurrent defi ciencies
of both may contribute to the etiologies of Kashin–
Beck disease in Russia, China, and Tibet, and myxede-
matous congenital hypothyroidism in Zaire. In addi-
tion, both nutrients are required for normal repro-
duction, normal gene expression, synthesis of zeno-
biotic and metabolizing enzymes in the liver, and
normal tolerance against cold stress. It is possible that
hypothyroidism associated with suboptimal selenium
status may explain some of the etiology of cardiovas-
cular disease and certain cancers.
Hypothyroidism is associated with defi ciencies of
other trace elements, including zinc, iron, and copper,