Table 2.

Summary of proposed mechanisms for functional dyspepsia.

Pathogenesis	Proposed mechanism
Abnormal gastrointestinal motility	(i) Abnormal accommodation of gastric fundus [6] (ii) Delayed gastric emptying [7] (iii) Rapid gastric emptying [8]
Visceral hypersensitivity	(i) Increased sensitivity to mechanical stimulation (gastric dilation) [9] (ii) Increased sensitivity to chemical stimulation (gastric acid or bile) [10]
Genetic factors	(i) Increased risk of FD in patients with polymorphism of G-protein b3 (GNB3) gene [11] (ii) Increased risk of PDS subtype of FD with polymorphism of serotonin transporter protein (SERT) gene [12] (iii) Increased risk of EPS subtype of FD with polymorphism of migration inhibitory factor (MIF) gene [13] (iv) Increased risk of EPS subtype of FD with polymorphism of regulated upon activation of normal T cells expressed and secreted (RANTES) gene [14]
H.  pylori infection	Downregulation of miR-1 and miR-133 caused by H.  pylori infection [15]
Postinfectious causes	(i) Increased prevalence of dyspeptic symptoms after infectious gastritis [16] (ii) Increased expression of interleukin 1β [17] (iii) Increased infiltration of gastric mucosa with eosinophils, macrophages, and intraepithelial lymphocytes after infection [18]
Psychosocial factors	(i) Higher prevalence of psychological symptoms in patient with dyspepsia (ii) Stress-induced elevated levels of CRH and ACTH which can affect gastric emptying [19]
Other factors	(i) Environmental factors (ii) Dietary exposures