Observations on two mongoloid children, one having primary hypothyroidism and the other having primary hyperthyroidism, have been reported. Primary hypothyroidism in the mongoloid child, in each of the three cases reported to date, has been associated with uterine bleeding attributed to hormonal overlap in the pituitary feedback mechanism. The significance of this phenomenon is not clean. A total of sixteen cases of mongolism with hyperthyroidism have been described. There is no evidence that altered thyroid function plays a role in the clinical manifestations of mongolism, and significant alteration in thyroid function is uncommon among such patients. Both of the carrier protein systems responded to the stresses of the superimposed disease processes in these mongoloid children as they do in normal children. Specifically, the values for the erythrocytic uptake of 1-I131-triiodothyronine and thyroxine and the triiodothynonine binding capacities (Case 2 only) were all in the expected ranges for both thyroid derangements involved. Similarly, in Case 2, where an iron-deficiency anemia was also present, the increase in the iron binding capacity and presumably in the level of transferrin was on the order of that to be expected for the degree of iron deficiency. The response to stress of both carrier protein systems in Down's Syndrome suggests that protein synthesis of transferrin and TBG is normal.