Nutrients and dyspepsia: paradigms and reality

Abstract

Dyspepsia is a common disorder that presents as persistent or recurrent abdominal pain or discomfort in the upper abdomen and originates from organic or functional causes. Heterogeneous disorders, physiopathological, psychosomatic, sociocultural, demographic and genetic components have a great impact on its presentation. Physiopathological elements and the influence of nutrients on symptomatology are discussed to help establish clearer guidelines for treatment. Gastric emptying is affected by physiological, pharmacological and dietary factors and is translated into symptoms and signs such as anorexia, nausea, vomiting, weight loss and abdominal pain. Liquid or solid meals may cause early or delayed emptying, which is associated with symptoms of postprandial fullness. Abnormal glucose and electrolyte serum values may also cause transitory emptying delay. Fatty and acid nutrients have also been reported to aggravate symptoms of functional dyspepsia, especially after large meals. Studies have also pointed at food sensibility and the effect of Helicobacter pylori infection on gastric emptying in symptomatic patients. Patients may suffer antral hypomotility and total/partial postingestion pattern conversion. Spinal brain axis dysfunction caused by peripheral inflammation is associated with gastric dysmotility. An association between symptoms and functional polymorphisms is pending further clarification. It has been questioned whether the genotype is associated with a specific physiopathological mechanism, postinfectious functional disorders or psychological/social alterations. The treatment of dyspepsia is empiric and is directed at improving symptoms associated with alterations in emptying, postprandial accommodation, hypersensibility and hyperalgesia. Further studies are required to correlate symptoms with food kinetics at the initial postfood ingestion stages.