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 mg/l (31 to 91 mg/24 h). Sample iodine varied from 10 to 260 mg/l (20 to 161 mg/24 h). Crude urinary iodine varied more than estimated 24 h iodine excretion (population standard deviation 32 v. 26; individual standard deviation 29 v. 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.

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.

Abnormal maternal thyroid function in early pregnancy was associated with epilepsy, ASD, and ADHD in the child, but associations differed by subtypes of exposure and by child age and sex. More evidence on subtypes and severity of maternal thyroid function is needed, and alternative outcomes of child neurodevelopment may be warranted.

Objective: The iodine intake level in a population is determined in cross-sectional studies. A fraction of samples with iodine content below a certain level, e.g. 25 mg/l, may suggest iodine deficiency in part of the population. However, urinary iodine varies considerably from day to day and the fraction of low samples caused by dispersion remains unsettled. Design: A longitudinal study of 16 healthy men living in an area of mild to moderate iodine deficiency. Methods: We measured urinary iodine and creatinine concentrations, and serum TSH, total thyroxine (T 4 ), free T 4 index and total tri-iodothyronine (T 3 ) in samples collected monthly for 1 year. Results: Average urinary iodine excretion was 57.0 mg/l (49.1 mg/24 h (corrected for creatinine excretion)) and varied from 29 to 81 mg/l (28 to 81 mg/24 h) between participants. Individual samples varied between 10 and 260 mg/l, and the variation around the mean was 2.4 times larger when calculated for the 180 individual samples compared with the 15 average annual values (1.7 times larger for estimated 24 h iodine excretion values). The fraction of individual samples below 25 mg/l was 6.7% (7.2% ,25 mg/24 h), whereas none of the participants had average iodine excretion below 25 mg/l or 25 mg/24 h. Participants with average annual iodine excretion below 50 mg/24 h had a negative correlation between iodine excretion and TSH, whereas a positive correlation was observed when average annual iodine excretion was above this level. Conclusions: Seven per cent of individual urine samples indicated severe iodine deficiency without this being present in the group studied. Dispersion was reduced by 24% when using estimated 24 h urinary iodine excretion rather than urinary iodine concentration. Participants with moderate iodine deficiency (average annual urinary iodine excretion 25±50 mg/24 h) showed clear signs of substrate deficiency for thyroid hormone synthesis while participants with mild iodine deficiency (50±100 mg/ 24 h) did not.