What causes Goiter? -- Stubner

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I have just read a fascinating article from Germany on what causes goiter.

Goiter is an increase in size of the thyroid. Goiter is due to two basic things: (1) an increase in the number of cells -- hyperplasia and (2) an increase in the size of the cells -- hypertrophy.

What they discovered was that TSH mainly induces hypertrophy -- an increase in the size of the cells. On the other hand, hyperplasia -- the increase in the number of cells -- is regulated by the intracellular iodine content. Thus, there are two different but related mechanisms involved.

With iodine deficiency, TSH increases and results in an increase in the size of the cells. This effect is amplified if there are goitrogens involved. With iodine deficiency, there is also less intrathyroidal iodine and an increase in the number of cells.

Thus, once you have goiter, the recommended treatment must deal with both issues -- reduction of TSH and increase in iodine.

What they found was most effective in healing iodine-deficient goiter was iodide therapy:

"T3 therapy was able to reduce mean cell area size, but it could not abolish hyperplasia and could not restore the iodine content over the critical point.... In our experiments, administration of T3 together with iodide had no advantages in comparison to treatment with iodide alone."

However, if the goiter has developed from a long period of iodine deficiency, there may be autonomous nodules that have developed. In this case, the autonomous nodules do not self-regulate the amount of iodine, and if you give too much, these nodules will create excess hormones:

"These data indicate that iodine supplementation is the causal therapy for iodine-deficient goitre, because it abolishes not only hypertrophy but also hyperplasia of the glands and restores normal function and regulation. However, the use of this therapy in man is limited by thyroid autonomies, which develop during long-standing iodine deficiency in the thyroid. The only possible way of solving this problem effectively is to start with early iodine prophylaxis."

Hypertrophy and hyperplasia during goitre growth and involution in rats--separate bioeffects of TSH and iodine. Stubner D, Gartner R, Greil W, Gropper K, Brabant G, Permanetter W, Horn K, Pickardt CR., 1987. Germany. Abstract. "Goitre growth was investigated in rats receiving a low iodine diet (less than 0.1 microgram iodine/g) and either 1 g/l KClO4 or 1 g/l propylthiouracil (PTU), or a combination of KClO4 or PTU with 50.82 nmol/1 T3 in tap water for 3 weeks. To investigate goitre involution, rats with iodine-deficient goitres were treated for 3 weeks either with T3 (0.5 microgram T3/day = 0.768 nmol/day), iodide (0.5 or 2.7 micrograms KI/day) or a combination of T3 with both iodide doses. Histology together with total DNA distinguished between hypertrophy and hyperplasia of the gland. During goitre growth there was highly significant correlation between goitre weight and TSH serum level (r = 0.93, P less than 0.001). Thyroid total DNA, however, was only weakly correlated to TSH but was inversely related to the degree of iodine deficiency. During goitre regression, TSH levels were normalized, histological signs of hypertrophy had disappeared, and thyroid weight was nearly normalized in all therapy groups. Total DNA, however, was normalized only with 2.7 micrograms KI/day (95 +/- 18 micrograms DNA/gland), and still elevated in all other groups. The highest DNA levels were found under T3 therapy (143 +/- 21 micrograms DNA/gland) and under 0.5 microgram KI/day (161 +/- 19 micrograms DNA/gland). Reduction of total DNA was independent of TSH, but followed replenishment of the iodine content of the glands. We conclude that TSH mainly induces hypertrophy, whereas thyroid hyperplasia is mainly regulated by the intracellular iodine content." http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve & db=pubmed & dopt=Abstract & list_uids=3425165 & query_hl=1 & itool=pubmed_docsum

Zoe