Abstract
Autoimmune thyroid diseases (AITD), primarily Hashimoto's thyroiditis and Graves' disease, represent the most common organ-specific autoimmune disorders and remain a significant clinical challenge due to their chronic course, frequent comorbidities, and limited options for causal treatment. In recent years, increasing attention has been directed toward the gut microbiota as a potential modulator of immune tolerance and endocrine autoimmunity. Accumulating evidence suggests that alterations in gut microbial composition and function may contribute to immune dysregulation, intestinal barrier dysfunction, and low-grade inflammation observed in patients with AITD. This narrative review summarizes current knowledge on the role of gut microbiota in the pathophysiology of autoimmune thyroid diseases, with a particular focus on nutritional determinants and diet-based strategies for microbiota modulation. We discuss mechanisms linking diet, microbial metabolites, intestinal permeability, and immune responses relevant to thyroid autoimmunity. Special attention is given to dietary patterns, specific nutrients, and bioactive food components that may influence gut microbiota composition and function, including fiber, selenium, iodine, vitamin D, polyphenols, and probiotic-containing foods. From a clinical standpoint, the available evidence remains limited and largely heterogeneous, with most data derived from observational studies rather than interventional trials. Although growing interest surrounds diet-driven modulation of the gut microbiota, current findings do not support its use as an independent therapeutic approach in autoimmune thyroid diseases. Instead, dietary interventions may be best viewed as a complementary element of overall patient care. Well-designed prospective studies are still needed to determine whether such strategies can meaningfully influence disease course, to define which patients may benefit, and to translate these observations into practical, evidence-based dietary guidance. Future progress will depend on function-focused, phenotype-informed studies integrating microbiota readouts with clinically meaningful endocrine endpoints.