Festschrift for Sir

source of faecal iodine is endogenous thyroid hormone, a fraction of which is excreted into the bile (Myant, 1956). Further evidence for an endogenous origin of faecal iodine is obtained from balance studies in patients with abnormal thyroid function (Harrison et al., 1965a). Patients with thyrotoxicosis excrete significantly more iodine in the faeces than normal, ranging from 21 to 72 ,tg/ day on a low iodine intake. Patients with untreated hypothyroidism, on the other hand, excrete less iodine in the faeces than normal, 1-16 jig/day on the same intake. In patients with non-toxic goitre due to iodine deficiency, the faecal excretion of iodine is normal, so that losses of iodine by this route are important in producing iodine deficiency when the intake is very low. In severe iodine deficiency the urinary excretion of iodide by contrast falls to very low levels. It may be inferred from the studies described here that the levels of faecal and urinary iodine reflect the size of the two pools of iodine which circulate in the body outside the thyroid gland. Faecal iodine is derived from circulating organic iodine, a pool about 500 ,ug in size which is replenished by thyroid hormone secreted from the gland, while the source of urinary iodine is the smaller inorganic iodine pool of about 50 ,ug which is supplied by dietary iodine and by deiodination of thyroid hormone. Abnormalities of iodine metabolism affect each of these pools in different ways, which produce characteristic alterations in the pattern of balance studies. The intestine plays an important role in the body's economy of iodine in health and disease, and ability to measure iodine balance has enhanced our understanding of the complicated metabolism of this element.