The purposes of this study were to evaluate possible effects of lithium on thyroid function, determine the relationship among thyroid function, antibody levels, and demographic/clinical variables, and establish the prevalence of lithium-related goiter, clinical hypothyroidism, and thyroid antibodies. Forty-nine patients who had taken lithium for a minimum of 6 months were enrolled, as were 46 age- and sex-matched controls naive to lithium use. Blood was drawn to measure levels of total and free T3, T4, thyroid-stimulating hormone (TSH), and antimicrosomal and antithyroglobulin antibodies.' Thyroid volume was quantified on ultrasonography. Twenty-nine patients in the study group (59%) and 7 in the control group (15%) had goiter. Free T4 levels were significantly lower in the study group, and TSH levels were higher. Among lithium-treated patients, 12% had clinical hypothyroidism and 2% had subclinical hypothyroidism. Thyroid antibodies were present in 23% of the lithium group and 15% of the control group. No significant relationship was apparent among thyroid antibodies, thyroid volume, and clinical hypothyroidism. Our findings suggested that along with its goitrogenic effects, lithium inhibited thyroid function and led to clinical hypothyroidism. Older age, family history of thyroid disorders, and the presence of thyroid antibodies significantly influenced thyroid function in the present study.