Pro-Inflammatory Diet as a Stimulating Factor in Hashimoto's Thyroiditis: Relationship with Intestinal Dysbiosis

• DOI: https://doi.org/10.22533/at.ed.15951025110211

• Palavras-chave: Thyroiditis. Hashimoto. Nutritional

• Keywords: Thyroiditis. Hashimoto. Nutritional

• Abstract:

  Introduction: Hashimoto's thyroiditis (HT) is an autoimmune disease and the most common endocrine disorder that predominantly affects women of childbearing age. The pathogenesis of HT is related to the lymphocytic infiltration of T and B cells in the thyroid and the production of anti-thyroid antibodies. Intestinal bacteria regulate the immune response and the digestion of micronutrients, and dysbiosis can be a trigger for autoimmune diseases. Aim: To discuss the pro-inflammatory nutritional influence on patients with Hashimoto's thyroiditis. Methods: Bibliographic review of articles from the last 5 years, using the PubMed database, with descriptors and Boolean operator AND, "Hashimoto Thyroiditis", "Nutrition" published in English. The selection filter used was the relationship between Hashimoto's thyroiditis and nutritional influence. 205 articles were found, duplicates and those off topic being excluded, resulting in 6 as the basis. Results: HT is characterized by the production of anti-thyroid peroxidase and anti-thyroglobulin antibodies, leading to chronic inflammation that affects glandular function. Pro-inflammatory dietary factors promote worsening of HT by causing failure in the induction and regulation of thyroid autoimmunity, increasing intercellular adhesion-1 in thyroid cells, leading to monocyte infiltration and accelerated inflammation. Oxidative stress results in overproduction of free radicals and impaired antioxidant defense due to the high levels of protein and lipid oxidation products. However, intestinal imbalance can be reversed with anti-inflammatory foods that will provide measurable benefits. Conclusion: Pro-inflammatory foods play a significant role in the pathogenesis and progression of HT, promoting autoimmune exacerbation via gut dysbiosis and high levels of TSH and TTA in the thyroid.