The relationship between the iodine intake level of a population and the occurrence of thyroid diseases is Ushaped with an increase in risk from both low and high iodine intakes. Developmental brain disorders and endemic goiter caused by severe iodine deficiency may seriously deteriorate overall health status and economic performance of a population. Severe iodine deficiency with a median 24-hour urinary iodine excretion of the population below 25 μg needs immediate attention and correction. Less severe iodine deficiency with median urinary iodine excretion below 120 μg per 24 hours is associated with multinodular autonomous growth and function of the thyroid gland leading to goiter and hyperthyroidism in middle aged and elderly subjects. The lower the iodine intake, the earlier and more prominent are the abnormalities. At the other end of the spectrum, severely excessive iodine intake starting at median urinary iodine excretion levels around 800 μg per 24 hours is associated with a higher prevalence of thyroid hypofunction and goiter in children. A number of studies indicate that moderate and mild iodine excess (median urinary iodine >220 μ g per 24 hours) are associated with a more frequent occurrence of hypothyroidism, especially in elderly subjects. The exact mechanism leading to this has not been clarified, and more studies are needed to define the limits of excessive iodine intake precisely. Due to the frequent occurrence of thyroid disorders, proper monitoring and control of the population iodine intake level is a cost-effective alternative to diagnosing, therapy and control of the many individual cases of thyroid diseases that might have been prevented.

The iodine intake level in a population is determined in cross-sectional studies. Urinary iodine varies considerably and the reliability of studies of iodine nutrition and the number of samples needed is unsettled. We performed a longitudinal study of sixteen healthy men living in an area of mild to moderate iodine deficiency. Iodine and creatinine concentrations were measured in spot urine samples collected monthly for 13 months. From these data we calculated the number of urine samples needed to determine the iodine excretion level for crude urinary iodine and for 24 h iodine excretion estimated from age- and gender-specific creatinine excretions. We found that mean urinary iodine excretion varied from 30 to 87 μg/l (31 to 91 μg/24 h). Sample iodine varied from 10 to 260 μg/l (20 to 161 μg/24 h). Crude urinary iodine varied more than estimated 24 h iodine excretion (population standard deviation 32v. 26; individual standard deviation 29v. 21; Bartlett's test,P < 0·01 for both). The number of spot urine samples needed to estimate the iodine level in a population with 95 % confidence within a precision range of ± 10 % was about 125 (100 when using estimated 24 h iodine excretions), and within a precision range of ± 5 % was about 500 (400). A precision range of ± 20 % in an individual required twelve urine samples or more (seven when using estimated 24 h iodine excretions). In conclusion, estimating population iodine excretion requires 100–500 spot urine samples for each group or subgroup. Less than ten urine samples in an individual may be misleading.

Large variations exist in thyrotropin (TSH) and thyroid hormones in serum. The components of variation include preanalytical, analytical, and biologic variation. This is divided into between- and within-individual variation. The latter consists of circadian and seasonal differences although there are indicators of a genetically determined starting point. The ratio of within- to between-individual variation describes the reliability of population-based reference ranges. This ratio is low for serum TSH, thyroxine (T₄) and triiodothyronine (T₃) indicating that laboratory reference ranges are relatively insensitive to aberrations from normality in the individual. Solutions are considered but reducing the analytical variation below the calculated analytical goals of 7%, 5% and 12% for serum T₃, T₄, and TSH does not improve diagnostic performance. Neither does determination of the individual set-point and reference range. In practice this means that population-based reference ranges are necessary but that it is important to recognize their limitations for use in individuals. Serum TSH responds with amplification to minor alterations in T₄ and T₃. A consistently abnormal TSH probably indicates that T₄ and T₃ are not normal for the individual even when inside the laboratory reference range. This underlines the importance of TSH in diagnosis and monitoring of thyroid dysfunctions. Also, it implies that subclinical thyroid disease may be defined in purely biochemical terms. Under critical circumstances such as pregnancy where normal thyroid function is of importance for fetal brain development, subclinical thyroid disease should be treated. Even TSH within the reference range may be associated with slightly abnormal thyroid function of the individual. The clinical importance of such small abnormalities in thyroid function in small children and pregnant women for brain development remains to be elucidated.

Background: Iodine intake is often measured by a surrogate measure, namely urine iodine excretion as almost all ingested iodine is excreted in the urine. However, the methods for urine collection and the reporting of the results vary. These methods, and their advantages and disadvantages, are considered in this article. Summary: There are two main ways in which urine can be collected for iodine measurement. The first is the collection of urine over a period, usually 24 hours. The second is the collection of a spot urinary sample. Urinary iodine values can be expressed as the content or concentration and reported without modification or as a function of creatinine in the same sample. The 24-hour urine for iodine measurement is often considered as the “reference standard” for giving a precise estimate of the individual iodine excretion and thereby iodine intake. As 24-hour collections are difficult to perform for large number of persons, single spot urinary samples are preferable to the 24-hour urinary collections in population studies. The iodine concentration in urine depends on the intake of both iodine and fluid. This, and the fact that there is a considerable variability in the daily iodine intake, makes the iodine measurement in spot urine samples unreliable for evaluating individuals for iodine deficiency, though they can be used to screen for exposure to large amounts of iodine from sources such as amiodarone and certain radiographic contrast agents. In populations of at least 500 subjects, the median value of spot urinary iodine concentration is a reliable measure of the iodine intake in the population as there is a leveling out of the day-to-day variation in iodine intake and urinary volume. Expressing the urinary iodide concentration as a function of urinary creatinine is useful in correcting for the influence of fluid intake. When doing so, it is recommended to adjust for the age- and sex-specific creatinine excretion in the given population. Conclusion: In studies of iodine intake, the correct choice of the method for collecting urine and the format for expressing the results of urine iodine measurement is essential to avoid misinterpretation of data on the iodine status of a population or individuals.

Important interaction exists between thyroid function, weight control, and obesity. Several mechanisms seem to be involved, and in studies of groups of people the pattern of thyroid function tests depends on the balance of obesity and underlying thyroid disease in the cohort studied. Obese people with a normal thyroid gland tend to have activation of the hypothalamic-pituitary-thyroid axis with higher serum TSH and thyroid hormones in serum. On the other hand, small differences in thyroid function are associated with up to 5 kg difference in body weight. The weight loss after therapy of overt hypothyroidism is caused by excretion of water bound in tissues (myxoedema). Many patients treated for hyperthyroidism experience a gain of more weight than they lost during the active phase of the disease. The mechanism for this excessive weight gain has not been fully elucidated. New studies on the relation between L-T₃ therapy and weight control are discussed. The interaction between weight control and therapy of thyroid disease is important to many patients and it should be studied in more detail.