Practice points
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The primary priority in iodine nutrition is to avoid severe iodine deficiency with insufficient thyroid hormone production and to prevent developmental brain damage.
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Developmental risk is also present in moderate iodine
The classical understanding of the relationship between iodine intake and disease was that people would develop disease if their iodine intake were below a certain limit.5 Because natural foods and beverages contained little iodine in many parts of the world, many populations were affected by iodine deficiency disorders.6 On the other hand, even intake of relatively large amounts of iodine were considered well tolerated, with toxicity seen only if intakes were many-fold higher than the
Table 1 illustrates the spectrum of disorders that somehow depends on the iodine intake level of the population.
By far, the most serious defect that may be associated with abnormal iodine intake is developmental brain damage caused by severe iodine deficiency.11 In foetal life, brain development takes place over a long period, starting as early as a few weeks after conception and continuing during the first years after birth.12
The iodine necessary for thyroid hormone production by the mother,
Many studies have shown that severe iodine deficiency is associated with a high frequency of goitre and hypothyroidism in a population, and that frank cretinism and less severe intellectual impairment may be common in such populations5, 11 (Table 1).
The description of iodine deficiency as severe, moderate or mild was based on compilations of data such as illustrated in Fig. 1. It is the association between the frequency of goitre and the level of urinary iodine excretion in various population
Severe iodine deficiency may cause excessive hypothyroidism in a population because of lack of substrate for thyroid hormone production. However, mild-to-moderate iodine deficiency is not associated with hypothyroidism. On the contrary, it is associated with excess hyperthyroidism in the population.32 Apparently, at moderately low levels of iodine intake, the thyroid gland is able to compensate for this and keep thyroid hormone production normal. However, as discussed below, the price of
In many people, the thyroid gland is not tolerated well by the immune system, as illustrated by the frequent finding of lymphocytic infiltration of the gland. In autopsy studies of white (Caucasians) and black Americans as well as British white and Japanese, Okayasu et al.44, 45 demonstrated lymphocytic thyroid infiltration in about 40% of white females over 20 years of age and up to 50% in elderly women living in the USA and in the UK. This was around 20% of the white males. In the black
It is well established that individual patients with autoimmune thyroiditis may develop hypothyroidism when exposed to excess iodine.54 Considering the very frequent occurrence of thyroid autoimmunity in the population, it would be expected that a high iodine intake would be associated with a high frequency of subclinical (with elevated serum TSH but a free T4 estimate within the reference range) and overt (elevated TSH and low estimate of free T4) hypothyroidism, and this has indeed been
It is well documented that programmes directed to increase the iodine intake of iodine-deficient populations will eradicate endemic cretinism and endemic goitre.66 This is the background for international recommendations on iodine intake and for the many national iodine fortification programmes.
However, the international recommendation is also against an excessive increase in iodine intake of a population, and this should be monitored.66 This recommendation is based on the finding that an
One pertinent question when evaluating the association between current iodine intake and the epidemiology of disease in a population is to what degree a previous exposure to a different level of iodine intake (low or high) may have influenced the current occurrences of diseases. For example, brain damage caused by iodine deficiency in early life is not reversible, even if the iodine intake becomes normal.
An increase from low to normal iodine intake is associated with a reduction in thyroid size
Both low and high levels of iodine intake associate with an increase in the risk of disease in a population. Optimally, iodine intake of a population should be kept within a relatively narrow interval where iodine deficiency disorders are prevented, but not higher. The primary priority in iodine nutrition is to avoid severe iodine deficiency with insufficient thyroid hormone production and to prevent developmental brain damage. Developmental risk is also present in moderate iodinePractice points