Department of Psychiatry, Uskudar University, Umraniye, Istanbul, Turkey.
Vocational School of Health Services, Department of Medical Documentation and Secretariat, Uskudar University, Istanbul, Turkey.
Adv Exp Med Biol. 2020;1191:155-167. doi: 10.1007/978-981-32-9705-0_10.
Anxiety disorders are a complex set of illnesses in which genetic factors, particularly stress, play a role in the etiopathogenesis. In recent years, inflammation and intestinal microbiota have also been included in this complex network of relationships. The functions associated with tryptophan catabolism and serotonin biosynthesis have long been associated with anxiety disorders. Tryptophan catabolism progresses toward the path of the kynurenine in the presence of stress and inflammation. The catabolism of kynurenine is a pathway in which many enzymes play a role and a large number of catabolites with neuroactive properties occur. The body's serotonin biosynthesis is primarily performed by enterochromaffin cells located in the intestines. A change in the intestinal microbiota composition (dysbiosis) directly affects the serotonin biosynthesis. Stress, unhealthy nutrition, and the use of antibiotics cause dysbiosis. In the light of this new perspective, the role of dysbiosis-induced inflammation and kynurenine pathway catabolites activated sequentially come into prominence in the etiopathogenesis of anxiety disorders.
焦虑障碍是一组复杂的疾病，其中遗传因素，特别是压力，在发病机制中起作用。近年来，炎症和肠道微生物群也被纳入了这一复杂的关系网络。与色氨酸分解代谢和 5-羟色胺生物合成相关的功能长期以来一直与焦虑障碍有关。在压力和炎症的存在下，色氨酸分解代谢向犬尿氨酸途径发展。犬尿氨酸的分解代谢是一个许多酶发挥作用的途径，并且会产生大量具有神经活性的代谢物。体内 5-羟色胺的生物合成主要由位于肠道内的肠嗜铬细胞完成。肠道微生物群组成的改变（失调）直接影响 5-羟色胺的生物合成。压力、不健康的营养和抗生素的使用会导致失调。从这个新的角度来看，在焦虑障碍的发病机制中，由失调引起的炎症和犬尿氨酸途径代谢物的级联激活作用突显出来。
