Goitre is prevalent in areas of iodine deficiency.A number of years ago one of us proposed that goitre is an adaptation to this deficiency (Stanbury et al., 1954), but this concept has been generalized and overinterpreted.The true adaptation to iodine deficiency is an increase in iodide clearance which is a consequence of higher blood flow and greatly enhaliced trapping of iodide.It was implicit in our concept that thyroid hyperplasia might be a means to that end and it is this latter extrapolation that we wish to analyse and refine.First, endemic goitre is often large and filled with colloid.Such goitres, because of insufficient iodination of thyroglobulin and leakage of iodide, aggravate the iodine deficiency.Secondly, there are several examples, both human and experimental, of excellent adaptation by higher trapping of iodide without significant thyroid enlargement.In fact, the ideally adapted thyroid would grow by a factor of no more than 2 (i.e. a small goitre) and comprise small hyperplastic follicles.The biochemistry of thyroglobulin synthesis, iodide trapping and organification, and thyroid hormone secretion may explain disordered and useless overgrowth of the well established endemic goitre, which in many aspects is maladapted. Goitre as a consequence of iodine deficiency and other nutritional causesEndemic goitre has long been recognized as a consequence of chronic iodine deficiency.Its eradication after the introduction of iodine prophylaxis proves this causal relationship.Other factors may further aggravate the consequences of iodine deficiency at the population level, among them goitrogens in the diet, e.g.thiocyanate from cassava or brassica (Bourdoux et al., 1978;Delange, 1994), unknown factors (Vought et al., 1967), microbial and other contaminants in drinking water (Gaitan et al.,
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Dumont et al. (1995) studied this question.