Acute Effects of Red Chili, a Natural Capsaicin Receptor Agonist, on Gastric Accommodation and Upper Gastrointestinal Symptoms in Healthy Volunteers and Gastroesophageal Reflux Disease Patients.

The effects of chili on gastric accommodation (GA) in gastroesophageal reflux disease (GERD) patients have not been explored. METHODS: In total, 15 healthy volunteers (HV) and 15 pH-positive non-erosive GERD (NERD) patients underwent single-photon emission computed tomography after ingesting 2 g of chili or placebo in capsules in a randomized double-blind crossover fashion with a one-week washout period. GA was the maximal postprandial gastric volume (GV) after 250 mL of Ensure® minus the fasting GV. Upper gastrointestinal symptoms were evaluated by using a visual analog scale. RESULTS: NERD patients but not HV had significantly greater GA after chili compared to a placebo (451 ± 89 vs. 375 ± 81 mL, p < 0.05). After chili, the postprandial GVs at 10, 20, and 30 min in NERD patients were significantly greater than HV (10 min, 600 ± 73 vs. 526 ± 70 mL; 20 min, 576 ± 81 vs. 492 ± 78 mL; 30 min, 532 ± 81 vs. 466 ± 86 mL, all p < 0.05). In NERD, chili was associated with significantly less satiety, more severe abdominal burning (p < 0.05), and a trend of more severe heartburn (p = 0.06) compared to the placebo. In HV, postprandial symptoms after chili and placebo ingestion were similar (p > 0.05). CONCLUSIONS: Chili enhanced GA in NERD patients but not in HV. This suggests that the modulation of GA in NERD is abnormal and likely involves transient receptor potential vanilloid 1 (TRPV1) sensitive pathways.

Chili Peppers, Curcumins, and Prebiotics in Gastrointestinal Health and Disease.

There is growing evidence for the role of several natural products as either useful agents or adjuncts in the management of functional GI disorders (FGIDs). In this review, we examine the medical evidence for three such compounds: chili, a culinary spice; curcumin, another spice and active derivative of a root bark; and prebiotics, which are nondigestible food products. Chili may affect the pathogenesis of abdominal pain especially in functional dyspepsia and cause other symptoms. It may have a therapeutic role in FGIDs through desensitization of transient receptor potential vanilloid-1 receptor. Curcumin, the active ingredient of turmeric rhizome, has been shown in several preclinical studies and uncontrolled clinical trials as having effects on gut inflammation, gut permeability and the brain-gut axis, especially in FGIDs. Prebiotics, the non-digestible food ingredients in dietary fiber, may serve as nutrients and selectively stimulate the growth and/or activity of certain colonic bacteria. The net effect of this change on colonic microbiota may lead to the production of acidic metabolites and other compounds that help to reduce the production of toxins and suppress the growth of harmful or disease-causing enteric pathogens. Although some clinical benefit in IBS has been shown, high dose intake of prebiotics may cause more bloating from bacterial fermentation.

Outcome of biofeedback therapy in dyssynergic defecation patients with and without irritable bowel syndrome.

AIM: The Rome II and III diagnostic criteria for dyssynergic defecation require the exclusion of irritable bowel syndrome (IBS). To prospectively study whether the presence of IBS affects the outcome of biofeedback therapy in dyssynergic defecation patients. METHODS: Consecutive patients with dyssynergic defecation underwent biofeedback therapy. Dyssynergic defecation was diagnosed based on symptoms, anorectal manometries, balloon expulsion tests, and colonic transit studies. The defecation dynamics and balloon expulsion time were evaluated at the end of the biofeedback therapy in all patients. IBS symptoms were graded before and 4 weeks after the biofeedback therapy using a 4-point Likert scale. Failure of the biofeedback therapy was defined as <50% improvement of constipation symptoms, which were evaluated using a 10 cm long visual analog scale before and 4 weeks after biofeedback therapy. RESULTS: Fifty patients completed the study. The biofeedback therapy was successful in 30 patients. Twenty-nine patients fulfilled the Rome II criteria for IBS. Patients with or without IBS demonstrated similar responses to the biofeedback therapy (16 of 29 vs. 14 of 21, P>0.05). The disappearance of IBS symptoms was observed more frequently in patients with an improved defecation index compared with those with no improvement (8 of 12 vs 4 of 17, P<0.05). A high pretreatment constipation symptom score, a high rectal sensory threshold, and a delayed colonic transit time were associated with a poor treatment outcome. CONCLUSIONS: The presence of IBS in dyssynergic defecation did not affect the outcome of biofeedback therapy. In addition, treating dyssynergic defecation patients with IBS by biofeedback therapy improved both constipation and IBS symptoms.

Ginger reduces hyperglycemia-evoked gastric dysrhythmias in healthy humans: possible role of endogenous prostaglandins.

Acute hyperglycemia evokes gastric slow wave dysrhythmias via endogenous prostaglandin generation. Ginger exhibits slow wave antiarrhythmic effects in other models, but its actions on hyperglycemia-evoked gastric dysrhythmias are unexplored. We hypothesized that ginger prevents disruption of slow wave rhythm by acute hyperglycemia via inhibition of prostaglandin production but not its actions. Twenty-two healthy humans underwent fasting electrogastrography during hyperglycemic clamping to 250 to 290 mg/dl after double-blind placebo or ginger root (1 g). Responses were compared with the prostaglandin E1 analog misoprostol (400 microg). Dominant frequencies (DF) and the percentage of recording times in the bradygastric [0.5-2 cycles/min (cpm)], normal (2-4 cpm), and tachygastric (4-9 cpm) frequency ranges were analyzed. After placebo, hyperglycemia reduced normal 2 to 4 cpm activity from 94.4 +/- 2.6 to 66.0 +/- 10.4%, increased the DF from 2.96 +/- 0.04 to 4.09 +/- 0.45 cpm, and increased tachygastria from 2.0 +/- 1.4 to 29.3 +/- 10.7% (P < 0.05). Hyperglycemia effects on normal activity (77.3 +/- 8.3%), DF (3.46 +/- 0.37 cpm), and tachygastria (15.6 +/- 8.6%) were significantly reduced by ginger (P < 0.05). Misoprostol evoked decreases in normal activity from 95.4 +/- 2.0 to 81.7 +/- 3.0% and increases in tachygastria from 3.1 +/- 1.6 to 11.2 +/- 2.4% (P < 0.05). However, ginger did not correct these abnormalities versus placebo (P = N.S.). In conclusion, acute hyperglycemia evokes gastric slow wave dysrhythmias that are prevented by ginger root. Conversely, the compound has no effect on dysrhythmias elicited by a prostaglandin E(1) analog, indicating that ginger likely acts to blunt production of prostaglandins rather than inhibiting their action. These findings suggest novel mechanisms for the traditional Chinese herbal remedy ginger.