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Background-Life stress contributes to symptom onset and exacerbation in the majority of patients with irritable bowel syndrome (IBS) and functional dyspepsia (FD); research evidence is conflicting, however, as to the strength of these effects. Aims-To test prospectively the relation of chronic life stress threat to subsequent symptom intensity over time. Patients-One hundred and seventeen consecutive outpatients satisfying the modified Rome criteria for IBS (66% with one or more concurrent FD syndromes) participated. Methods-The life stress and symptom intensity measures were determined from interview data collected independently at entry, and at six and 16 months; these measures assessed the potency of chronic life stress threat during the prior six months or more, and the severity and frequency of IBS and FD symptoms during the following two weeks. Results-Chronic life stress threat was a powerful predictor of subsequent symptom intensity, explaining 97% of the variance on this measure over 16 months. No patient exposed to even one chronic highly threatening stressor improved clinically (by 50%) over the 16 months; all patients who improved did so in the absence of such a stressor. Conclusion-The level of chronic life stress threat predicts the clinical outcome in most patients with IBS/FD. (Gut 1998;43:256-261) Keywords: irritable bowel syndrome; chronic life stress threat; symptom intensityIn irritable bowel (IBS) and functional dyspepsia (FD) syndromes, major life stress situations precede onset and/or exacerbation of symptoms, 1-3 and early observations suggest that symptoms either disappear or improve following resolution of major life stress problems. 4 Furthermore, an impressive and sustained improvement in symptoms occurs following the acquisition of more eVective stress management skills.5-7 In a recent study of patients with functional gastrointestinal disorders (FGID), 8 we showed a significant correspondence between the intensity of chronic life stress threat and the severity and extent of aVective, gastrointestinal, and extraintestinal symptomatology, particularly in patients with IBS-FD syndromes. Despite these observations, the extent to which life stress contributes to the course of IBS and/or FD symptoms remains uncertain. 10To extend our previous cross sectional findings, our aim was to examine, in patients with IBS, group and individual patterns of change in life stress and symptom intensity over time. Specifically we aimed to determine within subject: (1) covariance of life stress and subsequent symptom intensity over three time frames; (2) time lag relations (with and without relevant covariates); (3) the role of personality, age, sex, and emotional distress in the above; (4) the life stress predictors of any improvement or lack of improvement in symptom intensity over time; and (5) the life stress predictors of clinical (50% or more) improvement or no clinical improvement in symptom intensity over time. We hypothesised that: (1) life stress and subsequent symptom intensity will...

SUMMARY The effects of rectal distension on upper gastrointestinal motility were investigated in six healthy subjects. On a control day, gastric and duodenal motor activity was recorded for nine hours of fasting and for four hours after a meal, duodeno-caecal transit being assessed in both interdigestive and digestive states. Motor activity and transit were also measured on a test day during which the rectum was distended for one hour during fasting and for one hour postprandially. Control and test days were randomised. During fasting, rectal distension increased the incidence of migrating motor complexes (0-8±0O3 v 0-5+±02 h-'; p<0-01) and reduced the duodenal phase 2 motility index to 66±45% of that observed on the control day (p<0O01). Further, duodeno-caecal transit time was increased by rectal distension (99±30 v 71±35 min; p<0.05). Postprandially, the period of rectal distension was marked by a reduction in the duodenal motility index to 24±13% of that observed during the comparable period on the control day (p<0-001) and a concomitant increase in duodeno-caecal transit time (113±22 v 80+17 min; p<0-01). We conclude that upper gastrointestinal motor activity, the effector of luminal transit, may be profoundly influenced by stimulation of distal afferents.In the investigation of patients with functional bowel disorders, disturbances of upper gastrointestinal motility have been shown in association with colorectal dysfunction as manifested by altered patterns of defecation. "-Although this may reflect a widespread disorder of gastrointestinal smooth muscle, inappropriate activation of enteroenteric reflexes4 may also occur. Early animal studies showed that gastric7 and small intestinal motor activity67 could be inhibited by rectal distension, the rapidity of the response suggesting a predominantly neural mechanism. More recent studies confirm these findings and suggest that both splanchnic and vagal components participate in this reflex.'In man, different patterns of gastric and small intestinal motor activity occur during the interdigestive and digestive states.9 Throughout fasting, a period of intense regular contractile activity recurs

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We compared in humans simultaneous motor responses of the jejunum, ileum, proximal colon, and gallbladder (GB) to intravenous cholecystokinin octapeptide (CCK-OP). To gauge the physiological relevance of the doses of CCK-OP, intestinal motility and GB contraction were also quantified after a fatty meal. Eight healthy volunteers participated in both experiments. Six graded, 30-min intravenous infusions had a mean range of 2.2 to 73.2 pmol X kg-1 X h-1 of CCK-OP; these spanned from subphysiological (negligible contraction of GB) to pharmacological (producing intestinal symptoms and a 70-99% contraction of GB) levels. CCK-OP inhibited interdigestive cycles of motility, though in some persons fasting patterns persisted with doses of CCK-OP, which produced up to 50% reduction in GB volume. Motility indices of the ileum and proximal colon responded to CCK-OP by decreasing initially but then increasing with larger doses; motility of the jejunum increased gradually at all doses. Judged by the gallbladder's response to food (reduction in volume down from 74 to 29% of original volume), the physiological range of infused CCK-OP was approximately 5-16 pmol X kg-1 X h-1. Within this range of doses of CCK-OP, motility of the jejunum increased, whereas motility of the proximal colon was reduced. These data are consistent with CCK being a "physiological" mediator of intestinal motility in humans; responses of the intestine to the peptide appear to vary regionally.