Summary: Functional dyspepsia is characterized by the presence of at least one of the following symptoms: bothersome postprandial fullness, early satiation, epigastric pain, and epigastric burning that are unexplained after a routine clinical evaluation. Two main subtypes of functional dyspepsia include postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). The pathophysiology of functional dyspepsia is multifactorial. Gastrointestinal dysmotility seems to play a main role in PDS, while visceral hypersensitivity in EPS. Nowadays, there is a growing body of evidence supporting a new pathogenetic model of the disease based on the key role of duodenal disturbances, such as duodenal inflammation and eosinophilia linked to increased mucosal permeability, abnormal response to duodenal acid and lipids, and duodenal dysbiosis. Post-infectious activation of mucosal immune system is an established risk factor for functional dyspepsia. Alterations in duodenogastric reflexes may result in sensory-motor dysfunction of the stomach. Disturbances at the central nervous system level and psychological factors may also significantly contribute to the pathogenesis of this heterogenous disorder. Diagnosis is based on a careful clinical evaluation, testing for Helicobacter pylori and gastroscopy, when justified. Treatment includes education, reassurance, lifestyle and dietary recommendations, pharmacotherapy and psychotherapy. Herbal medicines are also frequently used by dyspeptic patients. Prokinetics are the first line treatment in PDS, and antisecretory drugs in EPS. Antidepressants and fundic relaxants are another option. Targeting low-grade duodenal inflammation, eosinophilia and dysbiosis, montelukast, histamine H1/H2 blockers and rifaximin were applied, but this promising new approaches require further testing.