This is a summary of an editorial by Fernando Azpiroz, MD, PhD *and Juan R. Malagelada, MD, PhD in the Gastroenterology ClinicsBloating -To some it is a subjective sensation of fullness or pressure inside the abdomen. To others, bloating means abdominal distensionSensation of Bloating: It could be 1)a hypersensitive abdominal wall that produces a sensation of increased abdominal tension 2)or the sensation may originate from hypersensitive abdominal viscera.e.g a) small bowel hypersensitivity that selectively affects mechanosensitive afferents, without disturbing normal perception of electrical stimulation b)there is increased perception of gastric distension in IBS'ersc)fundic distension also leads to the sensation of bloatingVisceral hypersensitivity is modulated by several mechanisms operating between the gut and the brain and this altered brain-gut communication may cause the sensation of bloatingThe tolerance of mechanical stimuli in the gut depends on muscular activity and compliance, on the number of receptors activated modified by the interaction of different stimuli in the gut . For instance, intraluminal gas is tolerated better within the colon than within the poorly compliant small bowel. Intestinal lipids, frequently related by patients to postprandial bloating, increase the sensitivity of the intestine to mechanical stimuli, Some data indicate that patients with IBS have increased sympathetic activity. Visceral perception also is known to be mediated at a cortical level and therefore may be influenced by cognitive mechanisms. MECHANISMS OF PHYSICAL ABDOMINAL EXPANSIONThe potential elements include adipose tissue (solid), fluid (endoluminal, intravascular, intraperitoneal), and endoluminal gas. Hwever fat accumulation, ascitis do not lead to bloating mostly.Abdominal bloating and distension may arise when tissular water content increases, as may occur with vascular ingurgitation and visceral edema. Also endoluminal fluid accumulation could lead to bloating. E.g 1)Accumulation of liquid in acute diarrheal conditions and in some cases of postprandial bloating2)An association between symptoms and arrival chyme( a mix ofsolid and liquid) has been shown to exist.3)The effect of fiber on bloating may be related to the luminal overload. 4)Accumulation of fecal content also may contribute to bloating, particularly in patients with constipation. The effect of gas on bloating is complicated as there are many factors that must be consider like 1)bloating and flatulence cannot be used interchangeably with each other. The ingestion of lactulose leads to flatulence but not always bloating. fiber has been shown not to affect flatulence but does affect blaoting. 2) The amout of gas produced depends on the amount of fermentable foodstuffs that remain unabsorbed in the small bowel and enter the colon, and the individual characteristics of the colonic flora. Exampleas are malabsorption disorders or SIBO. But Whether some degree of nutrient malabsorption plays a role in IBS has been disputed and exclusion diets are inconclusive In one study, even though Pimentel showed abnormal small intestinal flora by abnormal hudrogen breath tests in IBS'ers and normalization with neomycin there were no differences in another study in breath hydrogen concentration measured over 1 week were detected between healthy controls and IBS patients, although patients complained of significant bloatin.King et al concluded that ther were abnormal colonic flora because total hydrogen excretion increased in patients with IBS. This is further complicated by the fact that healthy subjects are able to propel and evacuate very large gas loads without perception of abdominal distension. 3)Propulsion and transit of intraluminal gas determine the times for diffusion into the blood and for bacterial consumption. Hence, the rate of gas transit is a critical factor that influences the volume and composition of gas in the different regions of the gut. What affects transit:1) tolerance to gas loads. In healthy people as much gas is infused in the GI tract, that much is evacuated upto 30 ml gas/min.Manometric studies detected no changes in phasic motor activity in response to slow infusion of gas in the small bowel . Gas infusion induces a tonic motor response: a contraction in the direction of the mouth to the infusion site and a relaxation distal to the collection site. Studies suggest that changes in tonic activity and capacitance of the gut due to distension may result in the displacement of large masses of luminal gas that offers low resistance to motion in healthy people. It has been shown that patients with bloating have impaired intestinal handling of gas loads due to impaired transit. This subtle motor dysfunction, which may lead to impaired propulsion and abnormal distribution of intraluminal contents, may explain the bloating, particularly in these patients who also have gut hypersensitivity and increased perception. 2)Reflexes also play a part in the transit of gas. Mild rectal distension provokes a reflex that leads to increased transit of gas in healthy people but not in IBS'ers.3)Retention of gas takes place by increased resistance to gas flow for exammple voluntary tightening of the anal spinchters and impaired intestinal propulsion. But regardless of anal function patients with bloating retain gas. In summary What has been discovered so far about abdominal distension and intolerance to gas loads:Abdominal distension depends on the volume of gas retained. But abdominal discomfort appears to derive from failure to propel gas, possibly because of uncoordinated intestinal motility rather than weak propulsion because studies have shown that weak propulsion leads to painless distension. It has been shown that the slowing effect of lipids is increased in patients with discomfort, whereas the prokinetic effect of distension is impaired markedly. The fact that neostigmine reduced gas retention and improved abdominal distension and symptom perception suggests that abnormal gas transit or perception of intestinal gas was responsible for the abdominal symptoms.Fourther studies have shown that there is impaired small intestinal propulsion but colonic transit is normal. Other possibilities"The hypothesis that abdominal bloating is caused by intestinal gas intolerance is attractive. Other possibilities, however, must be contemplated. For instance, individuals with increased gas production who are unable to evacuate gas because of anal incoordination and functional outlet obstruction may retain gas in the colon and eventually become symptomatic, and the same would apply to individuals who retrain gas evacuation because of social constrictions. Furthermore, functional dyspepsia frequently is associated to IBS, and in these patients postprandial bloating may originate in the stomach rather than in the intestine , . These patients exhibit impaired meal accommodation of the stomach and increased gastric perception . Thus, increased tension of the hypersensitive gastric wall, but not intestinal gas, may be the cause of dyspeptic bloating."THE POTENTIAL ROLE OF ABDOMINAL MUSCULAR ACTIVITYSome studies have measured girth changes in relation to bloating, and the results indicate that overall abdominal distension can be objectivated. Is the abdominal wall response the same in patients as in healthy subjects, however? A dystonic abdominal wall(that repeatedly contracts) could fail to support adequately intra-abdominal contents and make the patient feel bloated, particularly in the erect position. Protrusion of the abdominal wall can be produced by a redistribution of abdominal contents without net increments in intra-abdominal volume.