The American Thyroid Association recommends that adults be screened for thyroid dysfunction by measurement of the serum thyrotropin concentration, beginning at age 35 years and every 5 years thereafter. The indication for screening is particularly compelling in women, but it can also be justified in men as a relatively cost-effective measure in the context of the periodic health examination. Individuals with symptoms and signs potentially attributable to thyroid dysfunction and those with risk factors for its development may require more frequent serum thyrotropin testing.

Clinical studies have suggested that excess dietary iodine promotes autoimmune thyroiditis; however, the lack of a suitable animal model has hampered investigation of the phenomenon. In this study, different amounts of potassium iodide were added to the diets of chicken strains known to be genetically susceptible to autoimmune thyroiditis. Administration of iodine during the first 10 weeks of life increased the incidence of the disease, as determined by histology and the measurement of autoantibodies to triiodothyronine, thyroxine, and thyroglobulin. Further support for the relation between iodine and autoimmune thyroiditis was provided by an experiment in which iodine-deficient regimens decreased the incidence of thyroid autoantibodies in a highly susceptible strain. These results suggest that excessive consumption of iodine in the United States may be responsible for the increased incidence of autoimmune thyroiditis.

Evidence has been presented to support the idea that iodine plays an important role in autoimmune thyroiditis. Excessive amounts induce thyroiditis in genetically susceptible animal strains, while intrathyroidal depletion of iodine prevents disease in strains susceptible to severe thyroiditis. While the mechanisms by which iodine promotes thyroiditis is unknown, several hypotheses have been proposed. (1) T and/or B cells may react specifically to iodinated portions of thyroglobulin (Tg) so that severe iodine depletion renders Tg non-immunogenic. (2) A defect in the iodine processing machinery in thyroid epithelial cells of a susceptible person or animal may, in the presence of iodine, result in elevated levels of oxygen or iodine radicals, which could damage membrane lipids or proteins. (3) Defective iodine processing may result in the iodination of lipid or proteins (other than Tg) which could act either as immunogens or polyclonal activators.

Experiments were performed to analyze one mechanism by which elevated levels of dietary iodine may induce thyroglobulin (Tg) autoantibodies. We tested the hypothesis that highly iodinated Tg synthesized by animals fed a high iodine diet is significantly more immunogenic than Tg containing fewer iodine atoms. Cornell strain (CS) chickens, genetically susceptible to iodide-induced thyroiditis, were fed either a high or a low iodine diet. They were killed, and their thyroidal Tg was analyzed for iodine; the high iodine Tg (HI-Tg) had at least 60 and the low iodine Tg (LI-Tg) had less than 13 atoms/molecule of Tg. To determine if the degree of Tg iodination affected its immunogenicity, these Tg preparations were administered iv to normal chickens without adjuvants. Their sera were tested for antibodies by direct binding radioassays and RIAs. HI-Tg stimulated the synthesis of antibodies that reacted well with HI-Tg and the thyroid hormones T3 and T4, but only weakly with LI-Tg. The birds immunized with LI-Tg produced very little antibody to LI-Tg, T3, or T4, but a modest amount to HI-Tg. In other experiments, Tg autoantibodies found in chickens maintained on a high iodine diet similarly demonstrated enhanced binding to HI-Tg. The present studies show that HI-Tg is more immunogenic than LI-Tg and supports the hypothesis that a high iodine diet induces Tg autoantibodies by increasing the immunogenicity of the Tg molecule. In marked contrast with iodide-induced Tg antibodies, the Tg antibodies accompanying the severe and early-onset thyroiditis of obese strain chickens are to a large degree independent of dietary iodine intake.

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