Endemic Goiter in Western New Guinea. III. Thyroid-Stimulating Activity of Serum from Severely Iodine-Deficient People

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Abstract
People living in the Mulia Valley of Western New Guinea suffer from gross iodine deficiency. Goiter and associated defects (mental deficiency, motor abnormalities, deafness and deaf-mutism) are prevalent. Thyroid activity1 is increased and serum PBI values lie in the hypothyroid range despite clinical euthyroidism. Serum TSH levels in these people were measured by applying the McKenzie bioassay to unfractionated serum and serum concentrates. The mean level found in 23 nondefective people was about 3 μg MRC A/100 ml. This level is more than 100 times higher than that found in euthyroid New Zealand people and is about ⅕ of the mean level found in a group of hypothyroid New Zealand people. In 2 subjects treated with dried thyroid the serum TSH level was too low to detect (less than 0.3 μg MRC A/100 ml). In 4 subjects with mental deficiency, motor abnormalities, deafness or deaf-mutism the mean serum TSH level was not significantly different from that of the nondefective people. This is in accord with the previous finding that there was no essential difference in thyroid function between these 2 groups. No LATS was found in gammaglobulin concentrates of sera from the New Guinea people. The findings indicate that, in iodine deficiency which is severe enough to lower the serum PBI, the increased thyroid activity is indeed mediated by increased blood TSH levels. It remains to be established that the same mechanism operates in lesser degrees of iodine deficiency, in which serum PBI remains within normal limits. The virtual absence of clinical hypothyroidism in people having PBI values well in the hypothyroid range remains puzzling; though not apparent from our data, an increased proportion of triiodothyronine in thyroid secretion may offer an explanation. Thyrotoxicosis appearing when iodine deficiency is corrected (“Jod-Basedow” disease) probably arises in those few subjects who already have LATS in their blood. It is argued that during severe iodine deficiency the presence of LATS may not cause excessive thyroid hormone secretion.