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.

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.

Graves' disease is a common autoimmune disorder in women in fertile ages. The hyperthyroidism is caused by generation of TSH-receptor activating antibodies. In pregnancy both the antibodies and the antithyroid medication given to the mother pass the placenta and affect the foetal thyroid gland. Thyroid function should be controlled not only in the mother with Graves' hyperthyroidism but also in her foetus. The review includes two cases illustrating some of the problems in managing Graves' disease in pregnancy.Major threats to optimal foetal thyroid function are inadequate or over aggressive antithyroid drug therapy of the mother. It should be taken into account that antithyroid drugs tend to block the foetal thyroid function more effectively than the maternal thyroid function, and that levothyroxin (L-T 4 ) given to the mother will have only a limited effect in the foetus.Surgical thyroidectomy of patients with Graves' hyperthyroidism does not lead to immediate remission of the autoimmune abnormality, and the combination thyroidectomyCwithdrawal of antithyroid medicationCL-T 4 replacement of the mother involves a high risk of foetal hyperthyroidism. Conclusion: Antithyroid drug therapy of pregnant women with Graves' hyperthyroidism should be balanced to control both maternal and foetal thyroid function. Surgical thyroidectomy of a pregnant woman with active disease may lead to isolated foetal hyperthyroidism.

Subclinical hypothyroidism (SCH) is a common condition that is often observed without therapy. However, no evidence-based recommendation exists with regards to how patients with untreated SCH should be monitored. Monitoring involves regular assessment of symptoms and signs of hypothyroidism (HYPO) and biochemical tests of thyroid function. An important question when repeated tests of thyroid function are performed is how large a difference in test results is needed to be confident that the change is real and not just due to chance variation. Recent data show that the least significant difference between two tests in SCH is 40% for TSH and 15% for free thyroxine and free triiodothyronine, with 90% confidence. Furthermore, monitoring has to be based on biochemical function testing because serial evaluation of symptoms and signs related to HYPO is rather insensitive in detecting worsening of thyroid insufficiency. When the presence of thyroid peroxidase auto-antibodies (TPO-Ab) in serum has been demonstrated, repeated measurements do not add much useful information in the monitoring of individual subclinical hypothyroid patients, as levels of TPO-Ab vary in parallel with TSH in these patients. Lastly, we discuss how differences in the monitoring procedure influence the diagnostic outcome, and we suggest a follow-up approach for untreated subclinical hypothyroid patients.