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Advanced Nutrition and Dietetics in Gastroenterology
Abstract
Gastro-oesophageal reflux disease (GORD) is a common disorder affecting at least one in 10 of the population on a weekly basis, that is present when the return of gastric contents into the oesophagus causes symptoms or damages the mucosa. Twin studies have shown that inherited factors are responsible for 20–40% of the GORD and acquired factors, such as Helicobacter pylori infection, may play a role; however, recent reviews emphasise the importance of lifestyle and dietary factors as a cause of disease. A key difference between patients and healthy individuals is that transient lower oesophageal sphincter relaxations (TLOSRs) in the GORD patients frequently allow ‘reflux’ not only of air but also gastric acid and semi-digested food, leading to heartburn and regurgitation. In principle, any meal component that delays gastric emptying, stimulates acid secretion, impairs oesophageal function or increases sensitivity of the oesophagus to reflux worsens the severity of reflux related symptoms.
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Objective:
Weight gain is an important risk factor for gastroesophageal reflux disease (GERD); however, whether weight loss can lead to resolution of GERD symptoms is not clear. Our aim was to measure the impact of weight loss on GERD symptoms.
Design and methods:
In a prospective cohort study at a tertiary referral center, overweight/obese subjects (BMI 25-39.9 kg/m2) were enrolled in a structured weight loss program. Weight loss strategies included dietary modifications, increased physical activity and behavioral changes. At baseline and at 6 months, BMI and waist circumference were measured and all participants completed a validated reflux disease questionnaire.
Results:
A total of 332 adult subjects, mean age 46 years and 66% women were prospectively enrolled. At baseline, the mean body weight, BMI, and waist circumference were 101 (±18) kg, 35 (±5) kg/m2 and 103 (±13) cm. At 6 months, majority of the subjects (97%) lost weight (average weight loss: 13 ± 7.7 kg) and as compared with baseline, there was a significant decrease in the overall prevalence of GERD (15 vs. 37%; P < 0.01) and the mean GERD symptom score (1.8 vs. 5.5; P < 0.01). Overall, 81% of the subjects had reduction in GERD symptom scores; 65% had complete resolution and 15% had partial resolution of reflux symptoms. There was a significant correlation between % body weight loss and reduction in GERD symptom scores (r = 0.17, P < 0.05).
Conclusions:
In conclusion, the overall prevalence of GERD symptoms is high (37%) in overweight and obese subjects. A structured weight loss program can lead to complete resolution of GERD symptoms in the majority of these subjects.
Oesophageal mucosa dilated intercellular spaces (DIS) may be important for symptom perception in non-erosive reflux disease (NERD). Patients with NERD might have DIS even in the proximal oesophagus. We aimed to assess the effect of oesophageal perfusions with acid and weakly acidic solutions on 'exposed' and 'non-exposed' oesophageal mucosa and its relationship to symptoms in healthy subjects.
14 healthy volunteers underwent upper gastrointestinal endoscopy with biopsies at 3 and 13 cm proximal to the oesophagogastric junction (OGJ). In following sessions, subjects received 30 min perfusions with neutral, weakly acidic, acidic and acidic-bile acid solutions at 5 cm above the EGJ (separated 4 weeks). Biopsies were taken 20 min after perfusions. Electron microscopy was used to measure DIS. Subjects scored heartburn during perfusions using a visual analogue scale.
(1) Oesophageal perfusion with acid solutions, with or without bile acids, provoked DIS in the 'exposed' oesophageal mucosa; (2) oesophageal perfusion with weakly acidic solutions provoked identical changes to those observed after perfusion with acid solutions; (3) distal oesophageal perfusions not only provoked changes in the 'exposed' but also in the more proximal 'non-exposed' mucosa; and (4) in spite of the presence of perfusion-induced DIS, most healthy subjects did not perceive heartburn during the experiments.
The human oesophageal mucosa is very sensitive to continuous exposure with acidic and weakly acidic solutions. In spite of the presence of intraluminal acid and DIS, healthy subjects did not experience heartburn, suggesting that NERD patients should have other critical factors underlying their symptoms.
The psychological symptoms associated with binge eating disorder (BED) have been well documented. However, the physical symptoms associated with BED have not been explored. Gastrointestinal (GI) symptoms such as heartburn and diarrhea are more prevalent in obese adults, but the associations remain unexplained. Patients with bulimia have increased gastric capacity. The objective of the study was to examine if the severity of binge eating episodes would be associated with upper and lower GI symptoms.
Population-based survey of community residents through a mailed questionnaire measuring GI symptoms, frequency of binge eating episodes and physical activity level. The association of GI symptoms with frequency of binge eating episodes was assessed using logistic regression models adjusting for age, gender, body mass index (BMI) and physical activity level.
In 4096 subjects, BED was present in 6.1%. After adjusting for BMI, age, gender, race, diabetes mellitus, socioeconomic status and physical activity level, BED was independently associated with the following upper GI symptoms: acid regurgitation (P<0.001), heartburn (P<0.001), dysphagia (P<0.001), bloating (P<0.001) and upper abdominal pain (P<0.001). BED was also associated with the following lower GI symptoms: diarrhea (P<0.001), urgency (P<0.001), constipation (P<0.01) and feeling of anal blockage (P=0.001).
BED appears to be associated with the experience of both upper and lower GI symptoms in the general population, independent of the level of obesity. The relationship between increased GI symptoms and physiological responses to increased volume and calorie loads, nutritional selections and rapidity of food ingestion in individuals with BED deserves further study.
Currently, thickened feeds are increasingly being used to treat infants with gastroesophageal reflux, driven in large part by the baby food industry. Previous meta-analyses have shown that although thickened formulas do not seem to reduce measurable reflux, they may reduce vomiting. However, because data are limited, there is still uncertainty regarding the use of thickening agents.
Our goal was to systematically evaluate and update data from randomized, controlled trials on the efficacy and safety of thickened feeds for the treatment of gastroesophageal reflux in healthy infants.
The Cochrane Library, Medline, Embase, and CINAHL databases and proceedings of the European and North American pediatric gastroenterology conferences (from 2000) were searched in May 2008; additional references were obtained from reviewed articles. Only randomized, controlled trials that evaluated thickened feeds used in infants for at least several days for the treatment of gastroesophageal reflux were considered for inclusion. Three reviewers independently performed data extraction by using standard data-extraction forms. Discrepancies between reviewers were resolved by discussion between all authors. Only the consensus data were entered.
Fourteen randomized, controlled trials with a parallel or crossover design, some with methodologic limitations, were included. Use of thickened formulas compared with standard formula significantly increased the percentage of infants with no regurgitation, slightly reduced the number of episodes of regurgitation and vomiting per day (assessed jointly or separately), and increased weight gain per day; it had no effect on the reflux index, number of acid gastroesophageal reflux episodes per hour, or number of reflux episodes lasting >5 minutes but significantly reduced the duration of the longest reflux episode of pH<4. No definitive data showed that one particular thickening agent is more effective than another. No serious adverse effects were noted.
This meta-analysis shows that thickened food is only moderately effective in treating gastroesophageal reflux in healthy infants.
Gastric and duodenal bacterial overgrowth frequently occurs in conditions where diminished acid secretion is present. Omeprazole inhibits acid secretion more effectively than cimetidine and might therefore more frequently cause bacterial overgrowth.
This controlled prospective study compared the incidence of gastric and duodenal bacterial overgrowth in patients treated with omeprazole or cimetidine.
47 outpatients with peptic disease were randomly assigned to a four week treatment regimen with omeprazole 20 mg or cimetidine 800 mg daily. Gastric and duodenal juice were obtained during upper gastrointestinal endoscopy and plated for anaerobic and aerobic organisms.
Bacterial overgrowth (> or = 10(5) cfu/ml) was present in 53% of the patients receiving omeprazole and in 17% receiving cimetidine (p < 0.05). The mean (SEM) number of gastric and duodenal bacterial counts was 6.0 (0.2) and 5.0 (0.2) respectively in the omeprazole group and 4.0 (0.2) and 4.0 (0.1) in the cimetidine group (p < 0.001 and < 0.01; respectively). Faecal type bacteria were found in 30% of the patients with bacterial overgrowth. Basal gastric pH was higher in patients treated with omeprazole compared with cimetidine (4.2 (0.5) versus 2.0 (0.2); p < 0.001) and in patients with bacterial overgrowth compared with those without bacterial overgrowth (5.1 (0.6) versus 2.0 (0.1); p < 0.0001). The nitrate, nitrite, and nitrosamine values in gastric juice did not increase after treatment with either cimetidine or omeprazole. Serum concentrations of vitamin B12, beta carotene, and albumin were similar before and after treatment with both drugs.
These results show that the incidence of gastric and duodenal bacterial overgrowth is considerably higher in patients treated with omeprazole compared with cimetidine. This can be explained by more pronounced inhibition of gastric acid secretion. No patient developed signs of malabsorption or an increase of N-nitroso compounds. The clinical significance of these findings needs to be assessed in studies with long-term treatment with omeprazole, in particular in patients belonging to high risk groups such as HIV infected and intensive care units patients.
Visceral hypersensitivity is a feature of the irritable bowel syndrome (IBS). Postprandial symptoms are common in these patients. The effects of nutrients on colonic perception in IBS are incompletely understood.
We studied 13 healthy subjects and 16 patients with IBS-eight had diarrhoea predominant (IBS-D) and eight constipation predominant (IBS-C) IBS.
Colonic perception thresholds to balloon distension and viscerosomatic referral pattern were assessed before and after duodenal infusion of lipid or saline, respectively. At the end of the infusions, plasma levels of gastrointestinal peptides were determined.
Lipids lowered the thresholds for first sensation, gas, discomfort, and pain in the IBS group but only for gas in the control group. The percent reduction in thresholds for gas and pain after lipids was greater in the IBS and IBS-D groups but not in the IBS-C group compared with controls. IBS patients had an increased area of referred discomfort and pain after lipids compared with before infusion whereas the referral area remained unchanged in controls. No group differences in colonic tone or compliance were observed. In both groups higher levels of cholecystokinin, pancreatic polypeptide, peptide YY, vasoactive intestinal polypeptide, and neuropeptide Y were seen after lipids. Motilin levels were higher in patients and differences in the subgroups were observed. Levels of corticotrophin releasing factor were lower in the constipated group than in the diarrhoea group.
Postprandial symptoms in IBS patients may be explained in part by a nutrient dependent exaggerated sensory component of the gastrocolonic response.
The aetiology of gastro-oesophageal reflux is largely unknown. The authors' aim was to examine the relation between lifestyle habits and gastro-oesophageal reflux symptoms.
Participants of two consecutive public health surveys in Nord-Trondelag, Norway.
In a case control study within the two public health surveys, 3153 individuals who in the second survey reported severe heartburn or regurgitation during the last 12 months were defined as cases, while 40 210 people without reflux symptoms constituted the control group. The risk of reflux symptoms was estimated and multivariately calculated as odds ratios in relation to exposure to tobacco smoking, alcohol, coffee, tea, table salt, cereal fibres, and physical exercise.
There was a significant dose response association between tobacco smoking and reflux symptoms. Among people who had smoked daily for more than 20 years the odds ratio was 1.7 (95% confidence interval 1.5 to 1.9) compared with non-smokers. A similar positive association was found for table salt intake. The odds ratio for reflux was 1.7 (95% CI 1.4 to 2.0) among those who always used extra table salt compared with those who never did so. We found moderately strong negative associations between the risk of reflux and exposure to coffee, bread high in dietary fibre content, and frequent physical exercise. Intake of alcohol or tea did not affect the risk of reflux.
Tobacco smoking and table salt intake seem to be risk factors for gastro-oesophageal reflux symptoms. Dietary fibres and physical exercise may protect against reflux. Alcohol, coffee, and tea do not seem to be risk factors for reflux.
The incidence of oesophageal adenocarcinoma is increasing and the prognosis is poor. There is a strong predominance of white males, and heredity plays a minor role. The established risk factors are Barrett's oesophagus, gastro-oesophageal reflux, and obesity. Infection with Helicobacter pylori and use of non-steroidal anti-inflammatory drugs might reduce the risk. Medications that relax the lower oesophageal sphincter might contribute to increasing the risk. Among dietary factors, low intake of fruit, vegetables, and cereal fibres seem to increase the risk of oesophageal adenocarcinoma. The role of tobacco smoking is probably limited and alcohol consumption is not a risk factor. It is uncertain which factors cause the increasing incidence. Increasing prevalences of reflux and obesity, and decreasing prevalence of H pylori infection may contribute to this development; however, the sex distributions of these factors do not match the incidence trends well. Endoscopic surveillance for oesophageal adenocarcinoma among persons with reflux and obesity is discussed, but presently there is no evidence that strongly supports such a strategy.
Objective To update the findings of the 2005 systematic review of population-based studies assessing the epidemiology of gastro-oesophageal reflux disease (GERD).
Design PubMed and Embase were screened for new references using the original search strings. Studies were required to be population-based, to include ≥200 individuals, to have response rates ≥50% and recall periods <12 months. GERD was defined as heartburn and/or regurgitation on at least 1 day a week, or according to the Montreal definition, or diagnosed by a clinician. Temporal and geographic trends in disease prevalence were examined using a Poisson regression model.
Results 16 studies of GERD epidemiology published since the original review were found to be suitable for inclusion (15 reporting prevalence and one reporting incidence), and were added to the 13 prevalence and two incidence studies found previously. The range of GERD prevalence estimates was 18.1%–27.8% in North America, 8.8%–25.9% in Europe, 2.5%–7.8% in East Asia, 8.7%–33.1% in the Middle East, 11.6% in Australia and 23.0% in South America. Incidence per 1000 person-years was approximately 5 in the overall UK and US populations, and 0.84 in paediatric patients aged 1–17 years in the UK. Evidence suggests an increase in GERD prevalence since 1995 (p<0.0001), particularly in North America and East Asia.
Conclusions GERD is prevalent worldwide, and disease burden may be increasing. Prevalence estimates show considerable geographic variation, but only East Asia shows estimates consistently lower than 10%.
Regurgitated acid entering the mouth in gastro-esophageal reflux disease can cause dental erosion. Chewing gum could induce increased swallowing frequency, thus improving the clearance rate of reflux within the esophagus. The null hypothesis of this study was that chewing gum does not have any effect on the clearance of reflux from the distal esophagus. Thirty-one subjects presenting with symptoms of reflux were given a refluxogenic meal twice and were randomly selected to chew gum for half an hour after eating the meal. Esophageal pH was measured, and pH data were analyzed and compared during the postprandial periods for 2 hrs on the 2 occasions. The median (IQ range) values for the % time pH < 4 during the postprandial period without chewing gum were 5.7 (1.7-13.5) and, with chewing gum, 3.6 (0.3-7.3), respectively (p = 0.001). Chewing sugar-free gum for half an hour after a meal can reduce acidic postprandial esophageal reflux.
Gastro-oesophageal reflux disease (GORD) is present when the passage of gastric contents into the oesophagus causes symptoms or damages the mucosa. Potent suppression of gastric acid secretion with proton pump inhibitors is a highly effective and safe treatment for many patients with symptoms associated with reflux. It would be wrong to conclude, however, that proton pump inhibitors had solved the problem of GORD. The relation between reflux symptoms, endoscopic findings, and exposure of the oesophagus to acid is not straightforward. Some patients with a convincing history of heartburn fail to respond well to proton pump inhibitors. Although symptoms may be severe, at endoscopy the oesophagus is often found to be normal, and pH studies may not disclose the cause of symptoms that persist despite treatment for acid suppression.
Apart from typical symptoms of reflux many other problems have been linked to GORD, including dysphagia, hoarseness, non-cardiac chest pain, and chronic cough. It can, however, be difficult to identify those patients who will benefit from antireflux treatment. Most serious is the increased risk of oesophageal adenocarcinoma in patients with reflux symptoms, in particular those with Barrett's columnar lined oesophagus. Since the 1980s the incidence of oesophageal carcinoma has increased sixfold, more rapidly than any other common cancer.
#### Summary points
Gastro-oesophageal reflux disease (GORD) is common, causes a variety of symptoms, and is associated with important diseases, including asthma and oesophageal adenocarcinoma
Genetic influences and lifestyle factors such as smoking, obesity, and dietary behaviour may be involved in the development of GORD
The structure and function of the gastro-oesophageal junction is of key importance in reflux disease—as the condition becomes more severe, the risk of reflux during transient relaxations of the lower oesophageal sphincter rises and the volume of refluxate increases
Routine endoscopy is not required for reflux symptoms in the absence of features …
Lifestyle modifications are first-line therapy for patients with gastroesophageal reflux disease (GERD). We applied an evidence-based approach to determine the efficacy of lifestyle measures for GERD management. We used PubMed and Ovid to perform a search of the literature published between 1975 and 2004 using the key words heartburn, GERD, smoking, alcohol, obesity, weight loss, caffeine or coffee, citrus, chocolate, spicy food, head of bed elevation, and late-evening meal. Each study was reviewed by 2 reviewers who assigned one of the following ratings: evidence A, randomized clinical trials; evidence B, cohort or case-control studies; evidence C, case reports or flawed clinical trials; evidence D, investigator experience; or evidence E, insufficient information. We screened 2039 studies and identified 100 that were relevant. Only 16 clinical trials examined the impact on GERD (by change in symptoms, esophageal pH variables, or lower esophageal sphincter pressure) of the lifestyle measure. Although there was physiologic evidence that exposure to tobacco, alcohol, chocolate, and high-fat meals decreases lower esophageal sphincter pressure, there was no published evidence of the efficacy of dietary measures. Neither tobacco nor alcohol cessation was associated with improvement in esophageal pH profiles or symptoms (evidence B). Head of bed elevation and left lateral decubitus position improved the overall time that the esophageal pH was less than 4.0 (evidence B). Weight loss improved pH profiles and symptoms (evidence B). Weight loss and head of bed elevation are effective lifestyle interventions for GERD. There is no evidence supporting an improvement in GERD measures after cessation of tobacco, alcohol, or other dietary interventions.
Proton pump inhibitors (PPIs) may interfere with calcium absorption through induction of hypochlorhydria but they also may reduce bone resorption through inhibition of osteoclastic vacuolar proton pumps.
To determine the association between PPI therapy and risk of hip fracture.
A nested case-control study was conducted using the General Practice Research Database (1987-2003), which contains information on patients in the United Kingdom. The study cohort consisted of users of PPI therapy and nonusers of acid suppression drugs who were older than 50 years. Cases included all patients with an incident hip fracture. Controls were selected using incidence density sampling, matched for sex, index date, year of birth, and both calendar period and duration of up-to-standard follow-up before the index date. For comparison purposes, a similar nested case-control analysis for histamine 2 receptor antagonists was performed.
The risk of hip fractures associated with PPI use.
There were 13,556 hip fracture cases and 135,386 controls. The adjusted odds ratio (AOR) for hip fracture associated with more than 1 year of PPI therapy was 1.44 (95% confidence interval [CI], 1.30-1.59). The risk of hip fracture was significantly increased among patients prescribed long-term high-dose PPIs (AOR, 2.65; 95% CI, 1.80-3.90; P<.001). The strength of the association increased with increasing duration of PPI therapy (AOR for 1 year, 1.22 [95% CI, 1.15-1.30]; 2 years, 1.41 [95% CI, 1.28-1.56]; 3 years, 1.54 [95% CI, 1.37-1.73]; and 4 years, 1.59 [95% CI, 1.39-1.80]; P<.001 for all comparisons).
Long-term PPI therapy, particularly at high doses, is associated with an increased risk of hip fracture.
Background: Weight loss is commonly recommended as part of first-line management of gastro-oesophageal reflux disease (GORD) despite the paucity of published clinical trials. The aim of this study was to prospectively assess the independent effect of weight loss on reflux symptoms in overweight individuals with either normal endoscopic findings or grade-I oesophagitis. Methods: Thirty-four patients were recruited on the basis of a body mass index (BMI) of greater than 23 and symptoms of GORD for at least 6 months. All patients were advised to lose weight. Symptoms of gastro-oesophageal reflux (GOR) were scored, using a modified DeMeester questionnaire at 0, 6, and 26 weeks. Patients who were unable to stop taking all medication for control of symptoms were excluded from the study. Changes in weight and symptom score were analysed by using a paired t test. Correlation between change in weight and symptom score was assessed with the Pearson correlation test. Results: Thirty-four patients were studied (18 me...
OBJECTIVE:
Gastroesophageal reflux (GER) is increased in the right compared to the left recumbent position. Esophageal acid exposure is related to the acidity at the cardia, but the effect of body position on the acidity at the cardia has not yet been investigated. We aimed to investigate the mechanisms underlying increased esophageal acid exposure in the right recumbent position.
METHODS:
On 2 separate days a 4-h combined esophageal and lower esophageal sphincter (LES) manometry and pH recording of esophagus, gastric cardia, and corpus was performed in the right and left recumbent position after a high fat meal in 10 healthy subjects.
RESULTS:
In the right recumbent position a prolonged esophageal acid exposure (7.0% vs 2.0%, p < 0.03), a higher incidence of reflux episodes (3.8 vs 0.9/h, p < 0.03), more transient LES relaxations (TLESRs) (6.5 vs 3.2/h, p < 0.03), and higher percentage TLESRs associated with reflux (57.0% vs 22.4% p < 0.03) was recorded than in the left supine position. Acidity at gastric cardia and corpus was not affected by body position.
CONCLUSIONS:
Increased esophageal acid exposure in the right recumbent position relative to the left recumbent position is the result of a higher incidence of GER episodes caused by an increased incidence of TLESRs and higher percentage of TLESRs associated with GER. Body position does not affect the acidity at the gastric cardia and corpus.
PURPOSE: Gastroesophageal reflux disease is an important and increasingly common condition. Both overweight and high fat food consumption have been implicated as causes of reflux disease. We examined the relationship of overweight, high dietary fat intake, and other factors with reflux disease hospitalization.METHODS: We studied participants in the first National Health and Nutrition Examination Survey, a population-based sample examined in 1971–75 and followed through 1992–93. Persons with a physician-diagnosed hiatal hernia at baseline or reflux disease hospitalization within the first five years of study were excluded. A second analysis included follow-up of 9851 participants free of reflux disease in 1982–84. Ninety-six percent of the baseline cohort were recontacted. Reflux disease cases were persons hospitalized with a diagnosis of esophagitis or uncomplicated hiatal hernia. Hazard rate ratios for reflux disease hospitalization according to body mass index (BMI) (kg/m2), total daily servings of high fat foods and other factors were calculated using Cox proportional hazards analysis.RESULTS: A total of 12,349 persons were followed for a median of 18.5 years (range 5.0–22.1). Cumulative incidence of reflux disease hospitalization was 5.2% at 20 years. Multivariate survival analysis revealed higher reflux disease hospitalization rates with higher BMI (5 kg/m2) [hazard ratio (HR) = 1.22, 95% confidence interval (CI) = 1.13–1.32]. No relationship was found between higher fat intake and reflux disease hospitalization. Other factors associated with reflux disease hospitalization included age, low recreational activity, and history of doctor-diagnosed arthritis.CONCLUSIONS: Overweight, but not high dietary fat intake, increases risk of gastroesophageal reflux disease hospitalization.
BACKGROUND: Alginates form a raft above the gastric contents, which may suppress gastro-oesophageal reflux; however, inconsistent effects have been reported in mechanistic and clinical studies.
AIMS: To visualise reflux suppression by an alginate-antacid [Gaviscon Advance (GA), Reckitt Benckiser, UK] compared with a nonraft-forming antacid using magnetic resonance imaging (MRI), and to determine the feasibility of pH-impedance monitoring for assessment of reflux suppression by alginates.
METHODS: Two studies were performed: (i) GA and antacid (Alucol, Wander Ltd, Switzerland) were visualised in the stomach after ingestion in 12 healthy volunteers over 30 min after a meal by MRI, with reflux events documented by manometry. (ii) A randomised controlled, double-blind cross-over trial of post-prandial reflux suppression documented by pH-impedance in 20 patients randomised to GA or antacid (Milk of Magnesia; Boots, UK) after two meals taken 24 h apart.
RESULTS: MRI visualized a "mass" of GA form at the oesophago-gastric junction (OGJ); simple antacid sank to the distal stomach. The number of post-prandial common cavity reflux events was less with GA than antacid [median 2 (0-5) vs. 5 (1-11); P < 0.035]. Distal reflux events and acid exposure measured by pH-impedance were similar after GA and antacid. There was a trend to reduced proximal reflux events with GA compared with antacid [10.5 (8.9) vs. 13.9 (8.3); P = 0.070].
CONCLUSIONS: Gaviscon Advance forms a 'mass' close to the OGJ and significantly suppresses reflux compared with a nonraft-forming antacid. Standard pH-impedance monitoring is suitable for clinical studies of GA in gastro-oesophageal reflux disease patients where proximal reflux is the primary outcome.
In order to establish whether alcohol in amounts in amounts customarily imbibed during social drinking causes gastro-oesophageal reflux, 12 healthy young individuals, without symptoms of gastro-oesophageal reflux, were studied twice. Each time, distal oesophageal pH was monitored continuously for three hours after a standard meal which included either 180 ml 100 proof vodka or 180 ml water. The order of studies with and without alcohol was random. Peak blood alcohol concentrations ranged between 0.63 and 1.29 g/l. Eleven of the 12 subjects refluxed more after alcohol; and the difference in mean reflux scores for studies with and without alcohol was highly significant. We conclude that relatively modest quanttities of alcohol induce gastro-oesophageal reflux in healthy people.
We examined 66 patients with pain of possible esophageal origin for sensitivity to intraesophageal infusions of coffee, orange juice, spicy tomato drink, or HCl of varying concentrations as an addendum to their acid infusion (Bernstein) tests. Compared to Berstein-negative subjects, acid-sensitive patients were sensitive to infusion of coffee (P less than 0.01), orange juice (P less than 0.001), and tomato drink (P less than 0.001). Patients were largely insensitive to HCl solutions with a titratable acidity of 1 mEq per liter or less, less than the least acidic food solution tested. However, Berstein-positive patients were still highly sensitive to infusions of coffee, orange juice, and tomato drink adjusted to pH 7 (P less than 0.001). Patients were unable to differentiate symptoms caused by acid or food infusions, and solutions did not differ in the duration of infusion needed either to cause symptoms or to relieve them by saline. We conclude that the pain of esophagitis is nonspecific and can be precipitated by variety of seemingly unrelated substances.
The incidence and precipitating factors associated with symptomatic gastroesophageal reflux were evaluated by a questionnaire in 446 hospitalized and 558 nonhospitalized subjects. Of 385 control subjects 7% experienced heartburn daily, 14% noted heartburn weekly, and 15% experienced it once a month, giving a total of 36% of subjects having heartburn at least monthly. Daily heartburn occurred at a significantly greater (P less than 0.05) rate for 246 medical inpatients (14%) and for 121 patients seen in outpatient gastroenterological clinic (15%). Pregnant women seen in uncomplicated obstetrical clinic had symptoms of significantly greater (P less than 0.01) incidence: daily (25%) and at least once monthly (52%). Age, sex, or hospitalization did not significantly affect incidence. Fried foods, "spicy" foods, and alcohol were the most common precipitating factors.
Caffeine stimulates gastric acid secretion and reduces the competence of the lower esophageal sphincter in man. These effects of caffeine have been used as evidence that regular coffee should not be used by patients with peptic-ulcer disease or gastroesophageal reflux. We compared the dose-response relations of caffeine, regular coffee and decaffeinated coffee for gastric acid secretion and sphincter pressure in normal subjects. Decaffeinated coffee gave a maximal acid response of 16.5 +/- 2.6 mEq per hour (mean +/- S.E.M.), which was similar to that of regular coffee, 20.9 +/- 3.6 mEq per hour, both values being higher than that of caffeine, 8.4 +/- 1.3, on a cup-equivalent basis. Sphincter pressure showed minimal changes in response to caffeine, but was significantly increased by both regular and decaffeinated coffee (P less than 0.05). These data suggest that clinical recommendations based upon the known gastrointestinal effects of caffeine may bear little relation to the actual observed actions of coffee or decaffeinated coffee.
We studied the effects of an alginate compound (Gaviscon) on the frequency and the duration of gastroesophageal reflux (GOR) episodes in children. Twenty infants and children with characteristic symptoms of GOR were divided at random into two groups which were given either Gaviscon (ten patients, mean age: 21 months) or a placebo (ten patients, mean age: 35 months). A continuous pH probe monitoring of the lower oesophageal third was performed in all the patients before and after 8 days of treatment. Before the trial, sensitive pH monitoring variables of acid reflux (Euler-Byrne index, percentage of total reflux time per 24 h, mean duration and percentage of reflux time during sleep, total number of reflux episodes per 24 h and number of reflux episodes per 2 h post-cibal periods) were abnormal in all the patients tested. The oesophagram revealed a GOR in 13 of the 20 patients; none of the children who underwent an endoscopy had evidence of oesophagitis. Episodes of regurgitation reported by the parents decreased during Gaviscon therapy while no clinical improvement was noticed in the placebo group. No adverse effects were observed. After 8 days of treatment with Gaviscon, results of all the pH monitoring variables were significantly (P less than 0.05) reduced between -35% and -61% of the initial values recorded. In the placebo treated group, the mean values remained little changes (-9.5 to +8.2% of initial values). These data suggest that Gaviscon may prove useful in the medical management of GOR in infants and children.
In a randomized crossover study, we compared the effect on gastroesophageal reflux of three sleeping positions: elevation of the head of the bed on standard eight-inch bed blocks; elevation by a foam wedge; or a flat position. Fifteen subjects with moderate to severe reflux symptoms were studied in each position on consecutive nights using continuous intraesophageal pH monitoring. We found no difference in reflux frequency among the positions. The wedge caused a statistically significant decrease in the time that distal esophageal pH was less than 4 as compared to the flat position. The wedge also decreased the longest episode experienced by the subjects. Elevation on blocks caused a similar improvement in parameters but failed in this study to achieve statistical significance. Both elevation by a wedge and on blocks showed a trend towards a decrease in clearance time as compared to the flat position. The patients did not always prefer elevation on a wedge, but for some it is a valuable alternative to elevation by bed blocks.
Chocolate has been shown to decrease mean basal lower esophageal sphincter (LES) pressure, providing a rationale for the pathogenesis of chocolate-induced reflux symptoms. We assessed the relationship between chocolate ingestion and increased esophageal acid exposure using intraesophageal pH monitoring. Compared with ingestion of a dextrose control solution of similar volume, osmolality, and calories, postprandial ingestion of chocolate resulted in a significant increase in acid exposure in the first postprandial hour in patients with esophagitis. We conclude that this finding supports recommendations that patients with reflux esophagitis abstain from chocolate.
Individual l-amino acids were instilled intragastrically to determine possible differences in stimulation of gastric acid secretion and gastrin and pancreatic polypeptide release. Phenylalanine and tryptophan were significantly more potent stimulants of gastric acid secretion and of pancreatic polypeptide and gastrin release than any of the other amino acids tested. Smaller, but significant, responses were obtained with threonine for pancreatic polypeptide and with serine for acid secretion. We conclude that a major part of the acid-stimulating action of mixed amino acid solution can be explained by the aromatic amino acids, phenylalanine and tryptophan, which are also the most potent stimulants of gastrin and pancreatic polypeptide release. These studies suggest that the specific composition of amino acid mixtures determines the net effects of such mixtures on gastric secretion, and on release of both the antral hormone gastrin and the pancreatic hormone, pancreatic polypeptide.
Investigation of the motor events underlying gastroesophageal reflux has largely been confined to resting, recumbent subjects. The motor events associated with reflux during physical activity remain unknown. The aim of this study was to investigate the patterns of lower esophageal sphincter (LES) function underlying reflux in healthy subjects and the effect of exercise and physical activity on reflux mechanisms.
LES pressure was recorded with a perfused sleeve sensor in 10 healthy subjects; intraluminal transducers recorded pressure in the stomach, esophagus, and pharynx, and pH was recorded 5 cm above the LES. Signals were stored in a portable data-logger. Recordings were made for 24 hours, including moderate physical activity, periods of rest and sleep, standardized meals, and standardized exercise.
Most reflux episodes (81 of 123; 66%) occurred in the 3 hours after food intake; only 2 episodes occurred during exercise. LES pressure was < or = 3 cm H2O in 79% of reflux episodes. Transient LES relaxation was the mechanism of reflux in 82% of episodes, irrespective of activity or body position, whereas swallow-related LES relaxations accounted for 13% and persistently absent LES pressure accounted for 1%. Straining occurred in only 20% of episodes.
In ambulant healthy subjects, accurate continuous recording of LES function is possible, reflux usually occurs during transient LES relaxations, and straining is not a major factor in the induction of reflux.
Although many beverages produce heartburn, the relationship between the acidity and osmolality of beverages and heartburn is unclear. The aim of this study was to relate the acidity and osmolality of beverages with their ability to cause heartburn.
We measured pH, total titratable acidity, and osmolality of 38 beverages in vitro and then correlated acidity and osmolality with the amount of heartburn reported by questionnaire in 394 people with heartburn.
Among 17 citrus drinks and juices, titratable acidity correlated with reported heartburn scores (r = 0.65; P = 0.004). Soft drinks had the lowest pH readings of any beverages studied, and decreasing pH among soft drinks was correlated with reported heartburn scores (r = 0.82; P < 0.001). Alcoholic beverages (wines and beer), coffee, and (to a lesser extent) tea were associated with significant amounts of reported heartburn when compared with water. Milk was also associated with a modest amount of reported heartburn that was related to its fat content. Osmolality of beverages was unrelated to reported heartburn.
High titratable acidity of citrus drinks and juices and low pH of soft drinks are associated with more reported heartburn. Our findings provide a foundation for dietary advice in patients with heartburn and reflux esophagitis.
Patients with reflux disease often complain of heartburn after ingestion of coffee. Induction of gastro-oesophageal reflux has been demonstrated by pH-metry following the intake of coffee in healthy volunteers. The reflux was reduced when the coffee had undergone a decaffeination process. The aim of this study was to investigate the effect of decaffeination of coffee on reflux in patients with reflux disease.
Seventeen reflux patients underwent two osesophageal 3-h pH measurements. The patients received, in a double-blind study design in a randomized order, 300 mL of either regular or decaffeinated coffee together with a standardized breakfast. The fraction time oesophageal pH < 4 was calculated during the three postprandial hours.
For regular coffee the fraction time was calculated to a median of 17.9% with a range of 0.7-56.6%. The fraction time was significantly reduced to 3.1% (0-49.9%) after ingestion of decaffeinated coffee.
The amount of gastro-oesophageal reflux induced by the intake of regular coffee in patients with reflux disease can be reduce by the decaffeination of coffee.
Although fatty foods are commonly considered detrimental in patients with reflux disease, no objective data exist that substantiate this belief.
To investigate the effect of fat on gastro-oesophageal reflux and lower oesophageal sphincter (LOS) motor activity.
Thirteen healthy subjects and 14 patients with reflux disease.
Oesophageal pH, LOS, and oesophageal pressures were recorded for 180 minutes after a high fat (52% fat) and a balanced (24% fat) meal (both 3.18 MJ) on two different occasions. Eight controls and seven patients were studied in the recumbent position and the others in the sitting position.
The percentage of time at pH less than 4 and the rate of reflux episodes were higher (p < 0.01) in the patients than in the healthy subjects (mean 14.1% versus 1.7% and 4.4/h versus 0.8/h respectively), as was the percentage of transient LOS relaxations associated with reflux (62% versus 32%, p < 0.01). The high fat meal did not increase the rate of reflux episodes nor exposure to oesophageal acid in either group regardless of body posture. The rate of transient LOS relaxations, their association with reflux, and basal LOS pressure were also unaffected.
Increasing fat intake does not affect gastro-oesophageal reflux or oesophagogastric competence for at least three hours after a meal.
The reported effects of fatty meals on lower esophageal sphincter pressure (LESP) and gastroesophageal reflux (GER) are controversial. Therefore, the aim of the present study was to reevaluate the effect of isocaloric and isovolumetric low and high fat meals on LESP and GER.
Twelve healthy volunteers (six women, six men, 19 to 31 yr) received an isocaloric (842 kcal) solid-liquid (310 ml with 260 kcal) meal with either a low (10% fat, 14% proteins, 76% carbohydrates) or a high fat content (50% fat, 18% proteins, 32% carbohydrates) in a randomized, double-blinded fashion. The nutritional composition was identical for the solid and liquid part of the meals. In the first post-prandial hour LESP was recorded continuously using a Dent sleeve, and esophageal pH measurement was performed for 3 h postprandially with a glass electrode. We calculated the mean LESP, the frequency of transient LES relaxations (TLESR) and of reflux episodes (RE), the percentage of TLESR with GER, and the fraction time pH <4.
For all parameters measured no difference was observed between the low and the high fat meal. Mean LESP amounted to a median of 10.7 mm Hg (range, 7.3 to 15.1 mm Hg) after the low fat meal and to 11.1 mm Hg (5.2 to 16.3 mm Hg) after the high fat meal. The frequency of TLESR (n/1 h) rated to 9 (5 to 13) and 8 (4 to 14), and of RE (n/3 h) to 12 (3 to 22) and 11 (1 to 30). The percentage of TLESR with GER were 37% (0 to 100) and 30% (0 to 78). The fraction time pH <4 amounted to 2.3% (0.2 to 23.7) and 1.8% (0.1 to 28.8) after the low and high fat meal, respectively.
In healthy volunteers no difference in post-prandial LESP and GER was seen after a high fat meal compared with an isocaloric and isovolumetric low fat meal. Our results suggest that it is inappropriate to advise GER patients to reduce the fat content of their meals for symptom relief.
Weight loss is commonly recommended as part of first-line management of gastrooesophageal reflux disease (GORD) despite the paucity of published clinical trials. The aim of this study was to prospectively assess the independent effect of weight loss on reflux symptoms in overweight individuals with either normal endoscopic findings or grade-I oesophagitis.
Thirty-four patients were recruited on the basis of a body mass index (BMI) of greater than 23 and symptoms of GORD for at least 6 months. All patients were advised to lose weight. Symptoms of gastro-oesophageal reflux (GOR) were scored, using a modified DeMeester questionnaire at 0, 6, and 26 weeks. Patients who were unable to stop taking all medication for control of symptoms were excluded from the study. Changes in weight and symptom score were analysed by using a paired t test. Correlation between change in weight and symptom score was assessed with the Pearson correlation test.
Thirty-four patients were studied (18 men and 16 women) with a mean age of 65 years (range, 24-70 years). The mean weight at recruitment was 83.4 kg (standard deviation (s), 4.5 kg; BMI, 23.5 kg/m2 (s, 2.3 kg/m2). Twenty-seven patients (80% of the total) lost weight with a mean of 4.0 kg (P < 0.01) and improved by a mean reduction of 75% from the initial symptom score (P < 0.001). In nine patients the symptoms disappeared completely. Three patients gained weight and had a deterioration of their symptoms, whereas four patients gained weight but still improved their symptom score. There was a significant direct correlation between weight loss and symptom score (R = 0.548, P < 0.001).
This study has shown a significant association between weight loss and improvement in symptoms of GOR. Patients who are overweight should be encouraged to lose weight as part of the first-line management.
Spearmint is commonly used as an antispasmodic and as a flavouring in several medications including antacids. It can produce heartburn, presumably by lowering lower oesophageal sphincter (LES) tone, but the mechanism has not previously been objectively examined.
To study the effect of spearmint on LES function, acid reflux and symptoms.
In healthy volunteers, a Dent Sleeve and a pH electrode were placed in the distal oesophagus. They were then given spearmint either in a flavouring (0.5 mg), or a high (500 mg) dose, or a placebo, using a double-blind randomized crossover design. LES pressure, oesophageal pH and symptoms were recorded for 30 min before and after administration.
LES pressure was not affected by spearmint, either high dose (19.6 vs. 16.0 mmHg), flavouring dose (20.2 vs. 19.8 mmHg) or placebo (20.5 vs. 19.2 mmHg, all N.S.). There were no differences in reflux occurrence following high dose (mean = 0.65 vs. 0.85 episodes), low dose (0.4 vs. 0.5 episodes) or placebo (0.7 vs. 1.10 episodes, all N.S.). There was a significant increase in mean symptom scores following high-dose spearmint (0 vs. 0.35, P = 0.03), but not low dose (0 vs. 0.2) or placebo (0 vs. 0.5, both N.S.). One subject reported symptoms with placebo, one with low dose, and six with high dose; all without increased reflux episodes or decreased sphincter pressure.
Spearmint has no effect on LES pressure or acid reflux. Flavouring doses of spearmint do not produce more symptoms than placebo while high doses can be associated with symptoms, presumably from direct mucosal irritation but not reflux.
Gastroesophageal reflux (GER) is increased in the right compared to the left recumbent position. Esophageal acid exposure is related to the acidity at the cardia, but the effect of body position on the acidity at the cardia has not yet been investigated. We aimed to investigate the mechanisms underlying increased esophageal acid exposure in the right recumbent position.
On 2 separate days a 4-h combined esophageal and lower esophageal sphincter (LES) manometry and pH recording of esophagus, gastric cardia, and corpus was performed in the right and left recumbent position after a high fat meal in 10 healthy subjects.
In the right recumbent position a prolonged esophageal acid exposure (7.0% vs 2.0%, p < 0.03), a higher incidence of reflux episodes (3.8 vs 0.9/h, p < 0.03), more transient LES relaxations (TLESRs) (6.5 vs 3.2/h, p < 0.03), and higher percentage TLESRs associated with reflux (57.0% vs 22.4% p < 0.03) was recorded than in the left supine position. Acidity at gastric cardia and corpus was not affected by body position.
Increased esophageal acid exposure in the right recumbent position relative to the left recumbent position is the result of a higher incidence of GER episodes caused by an increased incidence of TLESRs and higher percentage of TLESRs associated with GER. Body position does not affect the acidity at the gastric cardia and corpus.
It is unclear whether fat digestion is required for the induction of gastrointestinal sensations and whether different fats have different effects. We investigated the effect of fat digestion and of medium-chain triglycerides (MCTs; C < 12) and long-chain triglycerides (LCTs; C > 16) on gastrointestinal sensations.
In a double-blind study, 15 healthy subjects were studied on 5 occasions during which LCT or MCT emulsions (2 kcal/min), with or without 120 mg tetrahydrolipstatin (THL, lipase inhibitor), or sucrose polyester (SPE, nondigestible fat) were infused intraduodenally in randomized order. After 30 minutes, the proximal stomach was distended in 1 mm Hg steps/min. Intensity of gastrointestinal sensations (on a 0-10 visual analog scale), plasma cholecystokinin (CCK) levels, and gastric volumes were assessed throughout.
LCT and MCT increased gastric volume at baseline pressure compared with SPE, and LCT more than MCT. THL entirely abolished this effect (volumes [mL]: LCT, 213 +/- 19; LCT-THL, 39 +/- 3; MCT, 155 +/- 12; MCT-THL, 43 +/- 5; SPE, 44 +/- 5). Only LCT increased plasma CCK levels (pmol/L per 30 minutes: LCT, 21 +/- 2; LCT-THL, 9 +/- 1; MCT, 9 +/- 1; MCT-THL, 11 +/- 1; SPE, 9 +/- 1). During distentions, intragastric volumes were greater during infusion of LCT and MCT than during the respective THL conditions or SPE, but plasma CCK levels did not change. The intensity of sensations increased (hunger decreased) more with LCT than with MCT. During infusion of THL or SPE, the effects were smaller than during LCT or MCT.
Fat digestion is required for the modulation of gastrointestinal sensations during gastric distention. The effects of fat depend on the fatty acid chain length and are not entirely explained by release of CCK.
Studies of the relative frequency of transient lower esophageal sphincter relaxations (TLESRs) in patients with gastroesophageal reflux disease and asymptomatic controls have revealed conflicting data. We have therefore studied the frequency of TLESRs and the frequency and mechanisms of acid reflux episodes in patients with gastroesophageal reflux disease and age- and sex-matched asymptomatic controls using standardized criteria.
Ten patients with symptomatic gastroesophageal reflux disease (four male, aged 50 [30-59] yr) and 10 asymptomatic matched volunteers (four male, aged 50 [32-59] yr) were studied. Esophageal, lower esophageal sphincter, and gastric manometric and esophageal pH readings were recorded for 1 h before and 1 h after a 200-kcal, 150 ml long-chain triglyceride meal.
TLESR frequency increased after the meal in both volunteers (median 0 [range = 0-3] to 3 [0-8] per hour,p < 0.01) and patients (1 [0-6] to 2.5 [0-9] per hour, p = 0.08). There was no significant difference in the frequency of TLESRs between volunteers and patients. TLESRs were more likely to be associated with acid reflux in patients (65% vs 37%, p = 0.03), whereas volunteers were more likely to reflux gas or liquid without acid (30% vs 3.0%, p = 0.01).
TLESRs are no more frequent in patients with gastroesophageal reflux disease than age- and sex-matched asymptomatic volunteers. However, when TLESRs occur in patients, they are twice as likely to be associated with acid reflux.
Colonic fermentation of carbohydrates is known to influence gastric and esophageal motility in healthy subjects. This study investigated the effects of colonic fermentation induced by oral administration of fructooligosaccharides (FOS) in patients with gastroesophageal reflux disease (GERD).
In the cross-over design used in the study, 9 patients with symptomatic GERD were administered a low-residue diet (i.e., 10 g fiber/day) during 2, 7-day periods, receiving either 6.6 g of FOS or placebo 3 times daily after meals. Each period was separated by a wash out of at least 3 weeks. On day 7, esophageal motility and pH were recorded in fasting conditions and after a test meal containing 6.6 g of FOS or placebo. Breath hydrogen concentrations (reflecting colonic fermentation) and plasma concentrations of glucagon-like peptide 1 (GLP-1), peptide YY, and cholecystokinin were monitored.
Compared with placebo, FOS led to a significant increase in the number of transient lower esophageal sphincter relaxations (TLESRs) and reflux episodes, esophageal acid exposure, and the symptom score for GERD. The integrated plasma response of GLP-1 was significantly higher after FOS than placebo.
Colonic fermentation of indigestible carbohydrates increases the rate of TLESRs, the number of acid reflux episodes, and the symptoms of GERD. Although different mechanisms are likely to be involved, excess release of GLP-1 may account, at least in part, for these effects.
In obesity, many gastro-oesophageal reflux promoting factors are present. Weight reduction is advised to symptomatic overweight subjects. The aim of the present study was to investigate the influences of untreated obesity, weight loss, and chronic gastric balloon distension on the lower oesophageal sphincter (LOS) function.
Patients entering a randomized, double-blind, sham-controlled study of balloon treatment, consisting of 4 months of either sham balloon or balloon treatment followed by 4 months of balloon treatment. Manometry and 24-hour pH measurements were performed at the start of the study and after 13 and 26 weeks.
Before treatment, LOS dysfunction was present in 7 of 32 patients (21.9%). Increased upright and supine reflux was present in 8 patients (25%). Sham treatment resulted in a weight loss of 9.7% with improved LOS function (a significant 0.6-cm increase in LOS length and a non-significant 2.6 mm Hg higher LOS pressure) and in a significantly decreased upright reflux (acid reflux time decreasing from 8.0 to 5.5% and number of meal-related and postprandial reflux episodes decreasing from 49 to 32). These improved values deteriorated after 4 months of balloon placement, with significantly increasing total, upright, and supine reflux to 7.5, 7.6, and 6.7% of the time, respectively, with oesophageal lesions after an overall 17.8% weight loss. Four months of balloon treatment induced a similar weight loss (9.9%) with significantly increased supine reflux from 1.6 to 6.7% of the time. After a second 4-month balloon period and an overall 13.8% weight loss, LOS and reflux values returned towards baseline values. A comparison of both groups demonstrated the adverse effects of balloon positioning after a period of substantial sham-induced weight loss.
Impaired LOS function and increased gastro-oesophageal reflux were observed in one quarter of the untreated obese subjects. Weight loss ameliorated manometry and pH values, but subsequent balloon positioning tended to counteract these beneficial changes. In patients on balloon treatment from the start, adverse effects seemed to wear off with prolonged treatment.
The postprandial increase of gastroesophageal reflux (GER) results largely from an increase in the rate of transient lower esophageal sphincter relaxations (TLESRs). Gastric distension is believed to be the most important contributing factor. The aim of this study was to determine the impact of rapid food intake on GER in healthy volunteers using combined multichannel intraluminal impedance and pH (MII-pH) testing to record both acid and nonacid reflux. Our hypothesis was that rapid food intake overstresses the gastric pressure-volume response and contributes to increased postprandial GER.
Twenty healthy volunteers were included in the study. On two separate days the participants were asked to eat the same standard meal within 5 or 30 min in random order. Acid and nonacid reflux episodes were recorded over a 2-h postprandial period.
Intake of a standard meal within 5 min was associated with more reflux episodes (median = 14) than an intake within 30 min (median = 10, p= 0.021). The increase was confined to the first postprandial hour and was caused predominantly by an increase of nonacid reflux. During the entire 2-h postprandial period, 469 reflux episodes were noted in the 40 studies. During the first postprandial hour 45% (135/303) of reflux events were nonacid as opposed to 22% (37/166) noted during the second hour (p < 0.0001).
Since rapid food intake produces more GER in healthy volunteers, studies in GERD patients are warranted to evaluate if eating slowly may represent another "life-style modification" aimed at reducing GER.
Body mass index (BMI) is a risk factor for gastro-oesophageal reflux but may simply be explained by diet and lifestyle.
We aimed to determine the contribution of BMI, diet and exercise to GER.
Community subjects (n = 211, mean age = 36 years, 43% males) completed validated questionnaires on gastro-oesophageal reflux, energy expenditure (Harvard Alumni Activity Survey), dietary intake (Harvard Food Frequency Questionnaire) and measures of personality and life event stress. Diet, exercise, BMI and other potential risk factors for reflux were analysed using logistic regression analyses.
The overall mean (+/- s.d.) BMI was 26.6 (+/- 5.7); 79 (37%) reported infrequent (< weekly) reflux and 16 (8%) reported frequent (> or = weekly) reflux. The median caloric intake was 2097 cal/day and the median daily energy expenditure was 1753 cal/day. Among those with BMI > 25, 10% reported frequent reflux compared to 4% of those with BMI < or = 25. In a model which included age, sex and Symptom Checklist-90 somatisation T-score, BMI was associated with reflux (OR per 5 units = 1.9, 95% CI: 1.2, 3.0). In models which included diet and exercise variables, BMI but not diet or exercise was associated with reflux.
BMI may be associated with symptomatic gastro-oesophageal reflux independent of diet and exercise.
Although diet has been associated with gastro-oesophageal reflux disease (GORD), the role of dietary components (total energy, macro and micronutrients) is unknown. We examined associations of GORD symptoms with intakes of specific dietary components.
We conducted a cross sectional study in a sample of employees (non-patients) at the Houston VAMC. The Gastro Esophageal Reflux Questionnaire was used to identify the onset, frequency, and severity of GORD symptoms. Dietary intake (usual frequency of consumption of various foods and portion sizes) over the preceding year was assessed using the Block 98 food frequency questionnaire. Upper endoscopy was offered to all participants and oesophageal erosions recorded according to the LA classification. We compared the dietary intake (macronutrients, micronutrients, food groups) of participants with or without GORD symptoms, or erosive oesophagitis. Stepwise multiple logistic regression analyses were used to examine associations between nutrients and GORD symptoms or oesophageal erosions, adjusting for demographic characteristics, body mass index (BMI), and total energy intake.
A total of 371 of 915 respondents (41%) had complete and interpretable answers to both heartburn and regurgitation questions and met validity criteria for the Block 98 FFQ. Mean age was 43 years, 260 (70%) were women, and 103 (28%) reported at least weekly occurrences of heartburn or regurgitation. Of the 164 respondents on whom endoscopies were performed, erosive oesophagitis was detected in 40 (24%). Compared to participants without GORD symptoms, daily intakes of total fat, saturated fat, cholesterol, percentage of energy from dietary fat, and average fat servings were significantly higher in participants with GORD symptoms. In addition, there was a dose-response relationship between GORD and saturated fat and cholesterol. The effect of dietary fat became non-significant when adjusted for BMI. However, high saturated fat, cholesterol, or fat servings were associated with GORD symptoms only in participants with a BMI >25 kg/m2 (effect modification). Fibre intake remained inversely associated with the risk of GORD symptoms in adjusted full models. Participants with erosive oesophagitis had significantly higher daily intakes of total fat and protein than those without it (p<0.05).
In this cross sectional study, high dietary fat intake was associated with an increased risk of GORD symptoms and erosive oesophagitis while high fibre intake correlated with a reduced risk of GORD symptoms. It is unclear if the effects of dietary fat are independent of obesity.
In the Western world at least, most upper gastrointestinal cancers now arise from the mucosa near to the oesophagogastric junction. Research into the mechanism of the development of adenocarcinoma at the oesophagogastric junction has mainly focused on the noxious effects of acid and bile. There is however an alternative concept for explaining the location of adenocarcinomas: the cancers are occurring at the anatomical site where saliva encounters acidic gastric juice and their interaction generates reactive nitrogen species which are potentially mutagenic and carcinogenic. At present, it is unclear whether the active nitrite chemistry is exerting detrimental effects on the surrounding tissue but it is important to investigate this possibility as it could reveal new ways of preventing and treating the high prevalence of disease occurring at this anatomical site.
Guidelines for the diagnosis and treatment of gastroesophageal reflux disease (GERD) were published in 1995 and updated in 1999. These and other guidelines undergo periodic review. Advances continue to be made in the area of GERD, leading us to review and revise previous guideline statements. GERD is defined as symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. These guidelines were developed under the auspices of the American College of Gastroenterology and its Practice Parameters Committee, and approved by the Board of Trustees. Diagnostic guidelines address empiric therapy and the use of endoscopy, ambulatory reflux monitoring, and esophageal manometry in GERD. Treatment guidelines address the role of lifestyle changes, patient directed (OTC) therapy, acid suppression, promotility therapy, maintenance therapy, antireflux surgery, and endoscopic therapy in GERD. Finally, there is a discussion of the rare patient with refractory GERD and a list of areas in need of additional study.
Recent reports suggest an increasing occurrence and severity of Clostridium difficile-associated disease. We assessed whether the use of gastric acid-suppressive agents is associated with an increased risk in the community.
To determine whether the use of gastric acid-suppressive agents increases the risk of C difficile-associated disease in a community population.
We conducted 2 population-based case-control studies using the United Kingdom General Practice Research Database (GPRD). In the first study, we identified all 1672 cases of C difficile recorded between 1994 and 2004 among all patients registered for at least 2 years in each practice. Each case was matched to 10 controls on calendar time and the general practice. In the second study, a subset of these cases defined as community-acquired, that is, not hospitalized in the prior year, were matched on practice and age with controls also not hospitalized in the prior year.
The incidence of C difficile and risk associated with gastric acid-suppressive agent use.
The incidence of C difficile in patients diagnosed by their general practitioners in the General Practice Research Database increased from less than 1 case per 100,000 in 1994 to 22 per 100,000 in 2004. The adjusted rate ratio of C difficile-associated disease with current use of proton pump inhibitors was 2.9 (95% confidence interval [CI], 2.4-3.4) and with H2-receptor antagonists the rate ratio was 2.0 (95% CI, 1.6-2.7). An elevated rate was also found with the use of nonsteroidal anti-inflammatory drugs (rate ratio, 1.3; 95% CI, 1.2-1.5).
The use of acid-suppressive therapy, particularly proton pump inhibitors, is associated with an increased risk of community-acquired C difficile. The unexpected increase in risk with nonsteroidal anti-inflammatory drug use should be investigated further.
An induction of gastro-oesophageal reflux has been reported after ingestion of alcoholic beverages in healthy volunteers. However, it is unknown whether reflux in gastro-oesophageal reflux disease patients will be enhanced by the ingestion of alcoholic beverages.
To investigate the effects of wine and beer on postprandial reflux in reflux patients.
Twenty-five patients (reflux oesophagitis 15, non-erosive reflux disease 10; 18 men and seven women) drank 300-mL white wine (n = 17), 500-mL beer (n = 8), or identical amounts of tap water (controls) together with a standardized meal in a randomized order. pH-measurement was carried out during three postprandial hours by pH-metry and the percentage of time pH < 4 was calculated.
Both alcoholic beverages increased reflux compared with water [wine 23% (median), water 12%, P < 0.01; beer 25%, water 11%, P < 0.05]. Between wine and beer, no difference in reflux induction was obtained. The reflux induction was seen in patients with (23%, P < 0.01) and without reflux oesophagitis (22%, P < 0.05) and in both sexes (women 23%, men 25%, P < 0.05 each).
Ingestion of commonly consumed alcoholic beverages such as wine and beer induces gastro-oesophageal reflux in gastro-oesophageal reflux disease patients. Therefore, these patients should be advised to avoid the intake of large amounts (> or = 300 mL) of these beverages.
Gastroesophageal reflux disease often occurs in patients with normal resting pressure and length of the lower esophageal sphincter. Such patients often have postprandial reflux. The mechanism of postprandial reflux remains controversial. To further clarify this, we studied the effect of carbonated beverages on the resting parameters of the lower esophageal sphincter. Nine asymptomatic healthy volunteers underwent lower esophageal sphincter manometry using a slow motorized pull through technique after ingestion of tap water and carbonated beverages. Resting pressure, overall length, and abdominal length of the lower esophageal sphincter were measured. All carbonated beverages produced sustained (20 minutes) reduction of 30-50% in all three parameters of the lower esophageal sphincter. In 62%, the reduction was of sufficient magnitude to cause the lower esophageal sphincter to reach a level normally diagnostic of incompetence. Tap water caused no reduction in sphincter parameters. Carbonated beverages, but not tap water, reduce the strength of the lower esophageal sphincter. This may be relevant to the pathogenesis of gastroesophageal reflux disease, especially in Western society.
A globally acceptable definition and classification of gastroesophageal reflux disease (GERD) is desirable for research and clinical practice. The aim of this initiative was to develop a consensus definition and classification that would be useful for patients, physicians, and regulatory agencies.
A modified Delphi process was employed to reach consensus using repeated iterative voting. A series of statements was developed by a working group of five experts after a systematic review of the literature in three databases (Embase, Cochrane trials register, Medline). Over a period of 2 yr, the statements were developed, modified, and approved through four rounds of voting. The voting group consisted of 44 experts from 18 countries. The final vote was conducted on a 6-point scale and consensus was defined a priori as agreement by two-thirds of the participants.
The level of agreement strengthened throughout the process with two-thirds of the participants agreeing with 86%, 88%, 94%, and 100% of statements at each vote, respectively. At the final vote, 94% of the final 51 statements were approved by 90% of the Consensus Group, and 90% of statements were accepted with strong agreement or minor reservation. GERD was defined as a condition that develops when the reflux of stomach contents causes troublesome symptoms and/or complications. The disease was subclassified into esophageal and extraesophageal syndromes. Novel aspects of the new definition include a patient-centered approach that is independent of endoscopic findings, subclassification of the disease into discrete syndromes, and the recognition of laryngitis, cough, asthma, and dental erosions as possible GERD syndromes. It also proposes a new definition for suspected and proven Barrett's esophagus.
Evidence-based global consensus definitions are possible despite differences in terminology and language, prevalence, and manifestations of the disease in different countries. A global consensus definition for GERD may simplify disease management, allow collaborative research, and make studies more generalizable, assisting patients, physicians, and regulatory agencies.