Celiac disease (CD) and Hashimoto’s thyroiditis (HT) frequently coexist, suggesting that shared mechanisms of autoimmunity extend beyond the intestine. In CD, the pathogenic role of gluten is firmly established; in HT, however, gluten is better viewed as a candidate modifier rather than a proven universal trigger. This review synthesizes current evidence on how gluten may influence the CD-HT axis through gut dysbiosis, epithelial barrier dysfunction, immune cross-reactivity, and epigenetic regulation. We also examine the clinical evidence for gluten-free diet (GFD) use in three settings: classical CD, CD-HT comorbidity, and HT without confirmed CD. Current data support lifelong GFD in CD and suggest that patients with both CD and HT may gain indirect thyroid-related benefit as intestinal inflammation improves. By contrast, evidence remains insufficient to recommend routine gluten withdrawal for all patients with non-celiac HT. Long-term GFD also carries practical and nutritional burdens that require professional supervision. Overall, the most defensible clinical approach is targeted screening for CD or other gluten-related disorders in selected HT patients, followed by individualized dietary counseling rather than universal restriction. Future work should prioritize mechanistically informed, adequately powered randomized trials to identify which thyroid-autoimmune phenotypes, if any, are most likely to benefit from gluten exclusion.
Fan et al. (Fri,) studied this question.