Inscrição na biblioteca: Guest
Portal Digital Begell Biblioteca digital da Begell eBooks Diários Referências e Anais Coleções de pesquisa
Critical Reviews™ in Biomedical Engineering

ISSN Imprimir: 0278-940X
ISSN On-line: 1943-619X

Critical Reviews™ in Biomedical Engineering

DOI: 10.1615/CritRevBiomedEng.2014011035
pages 17-24

GERD and Obesity: Is the Autonomic Nervous System the Missing Link?

Neranjani Devendran
Department of Medicine, McMaster University, Hamilton, Ontario, Canada
Nita Chauhan
Department of Pediatrics, Western University, London, Ontario, Canada
David Armstrong
Department of Medicine, McMaster University, Hamilton, Ontario, Canada
Adrian R. M. Upton
Division of Neurology, McMaster University Medical Centre, Room 4U6, 1200 Main Street West, Hamilton, Ontario, Canada L8N 3Z5
Markad V. Kamath
Department of Medicine, McMaster University, 1280 Main Street West, Hamilton, Ontario, L8N 3Z5 Canada


Gastroesophageal reflux disease (GERD) is a common chronic condition that not only impairs the quality of life of those who are affected by it but also poses a significant economic burden. It encompasses a wide spectrum of symptoms as a result of gastric content moving into the esophagus. The most common cause of GERD, other than a hiatus hernia, is considered to be transient lower esophageal sphincter relaxation. The lower esophageal sphincter (LES) normally has a higher resting tone than the stomach, thus preventing the reflux of gastric contents into the esophagus. The greater prevalence of GERD and GERD symptoms in obese individuals has generated significant interest in understanding the association between these 2 conditions and the underlying physiological mechanisms. The potential relationship between GERD and obesity and the exact mechanism by which obesity may cause reflux, however, remains uncertain. It has been proposed that patients with GERD have altered autonomic nervous function and, more specifically, have reduced parasympathetic activity. Obese individuals also have shown diminished parasympathetic activity, which may be reversed after weight reduction through exercise, diet control, and bariatric surgery. Given that contraction and relaxation of the LES are vagally mediated, the question that arises is whether the autonomic nervous system is, in fact, the missing link between obesity and GERD. In this article we examine the current evidence and hypothesize that the potential imbalance in sympathovagal stimulation to the LES is a key contributing factor to the increased prevalence of GERD symptoms in obese individuals.