Functional gastrointestinal disorders (FGIDs) are common and distressing. They are so named because a defined pathophysiology in terms of structural or biochemical pathways is lacking. Traditionally FGIDs have been conceptualized as brain-gut disorders, with subgroups of patients demonstrating visceral
hypersensitivity and motility abnormalities as well as psychological distress. However, it is becoming apparent that there are certain structural or biochemical gut alterations among subsets with the common FGIDs, most notably functional
dyspepsia (FD) and
irritable bowel syndrome (IBS). For example, a
sodium channel mutation has been identified in IBS that may account for 2 % of cases, and subtle intestinal
inflammation has been observed in both IBS and FD. Other research has implicated early life events and stress, autoimmune disorders and atopy and
infections, the gut microbiome and disordered mucosal immune activation in patients with IBS or FD. Understanding the origin of symptoms in FGIDs will allow
therapy to be targeted at the pathophysiological changes, not at merely alleviating symptoms, and holds hope for eventual cure in some cases. For example, there are promising developments in manipulating the microbiome through diet,
prebiotics and
antibiotics in IBS, and testing and treating patients for Helicobacter pylori
infection remains a mainstay of
therapy in patients with
dyspepsia and this
infection. Locally acting drugs such as
linaclotide have been an advance in treating the symptoms of
constipation-predominant IBS, but do not alter the natural history of the disease. A role for a holistic approach to patients with FGIDs is warranted, as brain-to-gut and gut-to-brain pathways appear to be activated.