Effect of obesity on esophageal transit*
References (21)
Chronic heart disease due to obesity
J Chronic Dis
(1965)- et al.
Relation of body weight to development of ischemic heart disease in a cohort of young North American men after a 26 year observation period: the Manitoba Study
Am J Cardiol
(1977) Gastroesophageal reflux and obesity
Surg Clin North Am
(1983)- et al.
Radionuclide transit: a sensitive screening test for esophageal dysfunction
Gastroenterology
(1981) - et al.
Indices of relative weight and obesity
J Chron Dis
(1972) - et al.
Esophageal scintigraphy to quantitate esophageal transit (quantitation of esophageal transit)
Gastroenterology
(1979) - et al.
Gastric emptying and obesity
Gastroenterology
(1983) - et al.
Overweight and hypertension
Circulation
(1969) - et al.
Weight and weight history in relation to cerebrovascular and ischemic heart disease
Arch Intern Med
(1971) The influence of obesity on health
N Engl J Med
(1974)
Cited by (64)
Surgical therapy of gastroesophageal reflux disease and obesity
2022, Obesity and Esophageal DisordersAssessment and management of gastroesophageal reflux disease following bariatric surgery
2021, Surgery for Obesity and Related DiseasesCitation Excerpt :GERD has a prevalence ranging from 40%–70% in the obese population while the incidence of hiatal hernias in the obese population ranges from 20%–53% [10,11]. The pathophysiology of GERD in obese patients is multifactorial and includes increased intra-abdominal pressure, altered LES competency, increased esophageal dysmotility, reduced esophageal acid clearance, and increased prevalence of hiatal hernias [12–14]. In addition, the evaluation of GERD is confounded by minimal correlation between symptoms of GERD and objective evidence of GERD [15].
The Gastrointestinal System and Obesity
2019, Dietary Interventions in Gastrointestinal Diseases: Foods, Nutrients, and Dietary SupplementsGastrointestinal Complications of Obesity
2017, GastroenterologyCitation Excerpt :Obesity increases the prevalence of esophageal motility disorders. For example, esophageal transit time was prolonged significantly in subjects with obesity compared with lean subjects,1 possibly because of increased gastric and gastroesophageal junction resistance.2 The typical abnormalities of esophageal motility are nonspecific abnormalities of esophageal peristalsis and, rarely, lower esophageal sphincter (LES) dysfunction, including isolated hypertensive or hypotensive LES pressures.
Esophageal abnormalities in morbidly obese adult patients
2016, Surgery for Obesity and Related DiseasesCitation Excerpt :One of the most probable mechanisms is the increase in mechanical stress imposed on the gastroesophageal junction and the predisposition to a hiatus hernia. Using high-resolution manometry techniques, it has recently been reported that obese patients are more likely to have gastroesophageal junction disruption, HH, and augmented intragastric pressure and gastroesophageal pressure gradient [41], confirming earlier studies [42–44]. In the present study, the HH prevalence was relatively low (12.5%) compared with that of other studies [8,33].
Role of Obesity in Barrett's Esophagus and Cancer
2009, Surgical Oncology Clinics of North AmericaCitation Excerpt :In this small case series, Roux-en-Y gastrojejunostomy resulted in complete or partial regression of BE in four of five patients with improvement in reflux symptoms in all. Obesity may contribute to gastroesophageal reflux through several anatomic and physiologic mechanisms (eg, increased intra-abdominal pressure and development of hiatus hernia,44 increased intragastric pressure and gastroesophageal sphincter gradient,45 slower esophageal transit times,46 and increased transient relaxations of the lower esophageal sphincter47). Few studies have distinguished between overall obesity and abdominal obesity, but one recent study showed a similar, albeit weak, positive correlation between the BMI and waist circumference and intragastric pressure.48
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Presented at the 25th Annual Meeting of the Society for Surgery of the Alimentary Tract, New Orleans, Louisiana, May 22–23, 1984.
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Dr. Mercer is Howard Wright Research Fellow in Diseases of the Esophagus and Cancer.