A B S T R A C T Since lithium has been showx%n to inhibit release of iodine from the thyroid, we have investigated its therapeutic potential in thvrotoxicosis. Eight detailed "lI kinetic studies were performed on seven thvrotoxic women and data was analy,zed using a computer program. Lithium at serum levels of about 1 mEq 'liter decreased the loss of '31I from the thyroid, led to a fall in serum "II levels and diminished urinary "'I excretion. Coinputer simulation of the lithium effect required, in every case, that lithium inhibit hormonal and( nonllormonal thyroid iodine release. In five cases a second lithium effect was required for a satisfactory fit of the model soluton with observed data: namely, an inhibition of hormone disappearance from serunm.Neither inhibition of release nor of hormone disappearance seemled to be affected by mlethimazole (release: 52% decrease without methimilazole, 60,% \w-ith mlethimazole; hormone disappearance: -60% decrease in both). Wlheni Li' was discontinued, recovery of the iodine release rate and hormiione disappearance rate over the observed time span -was variable, ranging from no recovery to rates that exceeded pre-Li' values. When Li' is used alone its effect on serum hormone levels is diminished due to continued accumulation of iodide by the thyroid. Thus, serum thyroxine-iodine levels fell 21-30% in 6-8 days in patients wlho did not receive methimazole and 15-67%C in the methimazoletreated subjects. For prolonged therapy, therefore, a thiocarbamide drug must be used in conjunction witlh Li'. The similarity of inhibition of iodine release from the thvroid produced by Li' and iodides is discussed.