Increased iodide intake has been linked to the development of hypothyroidism and/or autoimmune thyroiditis in humans and animals, but the mechanisms involved remain poorly understood. Increased ingestion of iodide is likely to have pleiotropic effects on either metabolic or immunological processes. Within the latter domain, recent interest has been focused on two areas: a) the role of iodinated peptides in thyroglobulin (Tg)--the molecular site of biosynthesis and storage of iodotyrosines and iodothyronines--in triggering an autoimmune cascade, and b) the role of iodine-induced apoptosis/necrosis of thyrocytes in the disease process. This review presents a brief summary of recent findings in these research areas.