pmc logo image
Logo of yjbmLink to Publisher's site

Formats:

Yale J Biol Med. 1999 Mar-Jun; 72(2-3): 69–80.
PMCID: PMC2579007
Defining GERD.
S. J. Sontag
VA Hospital, Hines, Illinois, USA.
Abstract
"It is not the death of GERD that I seek, but that it turns from its evil ways and follows the path of righteousness." The reflux world is fully aware of what GERD is and what GERD does. What the world does not know, however, is the answer to the most important yet least asked question surrounding GERD's raison-d'etre: Why is GERD here and why do we have it? What GERD is: abnormal gastric reflux into the esophagus that causes any type of mischief. What GERD does: causes discomfort and/or pain with or without destroying the mucosa; causes stricture or stenosis, preventing food from being swallowed; sets the stage for the development of esophageal adenocarcinoma; invades the surrounding lands to harass the peaceful oropharyngeal, laryngeal and broncho-pulmonary territories; reminds us that we are not only human, but that we are dust and ashes. Why GERD is here: We propose three separate and distinct etiologies of GERD, and we offer the following three hypotheses to explain why, after 1.5 million years of standing erect, we have evolved into a species (specifically Homosapiens sapiens) that is destined to live with the scourge of GERD. Hypothesis 1: congenital. The antireflux barrier, comprising the smooth-muscled lower esophageal sphincter, the skeletal-muscled right crural diaphragm and the phreno-esophageal ligament does not completely develop due to a developmental anomaly or incomplete gestation. Hypothesis 2: acute trauma: The antireflux barrier in adults suffering acute traumatic injury to the abdomen or chest is permanently disrupted by unexpected forces, such as motor vehicle accidents (with steering wheel crush impact), blows to the abdomen (from activities such as boxing, etc.), heavy lifting or moving (e.g., pianos, refrigerators) or stress positions (e.g., hand stands on parallel gym bars). The trauma creates a hiatal hernia that renders the antireflux mechanism useless and incapable of preventing GERD. Hypothesis 3: chronic trauma: The antireflux barrier in children and adults is gradually weakened over time as a result of chronic straining to defecate and straining in an unphysiologic position, both of which stem from our modern day habits of eating a low-fiber diet and living on the high-seated toilet. We suggest that the chronic traumatic hiatal hernia is (a) the cause of more than 90 percent of the GERD that stalks the Western world; (b) is a direct result of abandoning the popular and worldwide practice of squatting to socialize, eat and defecate; and (c) is our just reward for adopting the "civilized" high sitting position on chairs and modern toilets.
Full text
Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (1.6M), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References.
Images in this article
Click on the image to see a larger version.
Selected References
These references are in PubMed. This may not be the complete list of references from this article.
  • ALLISON PR. Reflux esophagitis, sliding hiatal hernia, and the anatomy of repair. Surg Gynecol Obstet. 1951 Apr;92(4):419–431. [PubMed]
  • Cohen S, Harris LD. Does hiatus hernia affect competence of the gastroesophageal sphincter? N Engl J Med. 1971 May 13;284(19):1053–1056. [PubMed]
  • Sontag SJ. Rolling review: gastro-oesophageal reflux disease. Aliment Pharmacol Ther. 1993 Jun;7(3):293–312. [PubMed]
  • Hill LD, Aye RW, Ramel S. Antireflux surgery. A surgeon's look. Gastroenterol Clin North Am. 1990 Sep;19(3):745–775. [PubMed]
  • Sontag SJ, Schnell TG, Miller TQ, Nemchausky B, Serlovsky R, O'Connell S, Chejfec G, Seidel UJ, Brand L. The importance of hiatal hernia in reflux esophagitis compared with lower esophageal sphincter pressure or smoking. J Clin Gastroenterol. 1991 Dec;13(6):628–643. [PubMed]
  • Mittal RK, Fisher MJ. Electrical and mechanical inhibition of the crural diaphragm during transient relaxation of the lower esophageal sphincter. Gastroenterology. 1990 Nov;99(5):1265–1268. [PubMed]
  • Mittal RK, Stewart WR, Schirmer BD. Effect of a catheter in the pharynx on the frequency of transient lower esophageal sphincter relaxations. Gastroenterology. 1992 Oct;103(4):1236–1240. [PubMed]
  • Darling DB. Hiatal hernia and gastroesophageal reflux in infancy and childhood. Analysis of the radiologic findings. Am J Roentgenol Radium Ther Nucl Med. 1975 Apr;123(4):724–736. [PubMed]
  • Astley R, Carré IJ, Langmead-Smith R. A 20-year prospective follow-up of childhood hiatal hernia. Br J Radiol. 1977 Jun;50(594):400–403. [PubMed]
  • al-Arfaj AL, Khwaja MS, Upadhyaya P. Massive hiatal hernia in children. Eur J Surg. 1991 Aug;157(8):465–468. [PubMed]
  • BOTHA GSM. The gastro-oesophageal region in infants; observations on the anatomy, with special reference to the closing mechanism and partial thoracic stomach. Arch Dis Child. 1958 Feb;33(167):78–94. [PMC free article] [PubMed]
  • LIGHT HG, ROUTLEDGE JA. INTRA-ABDOMINAL PRESSURE FACTOR IN HERNIA DISEASE. Arch Surg. 1965 Jan;90:115–117. [PubMed]
  • Fedail SS, Harvey RF, Burns-Cox CJ. Abdominal and thoracic pressures during defaecation. Br Med J. 1979 Jan 13;1(6156):91–91. [PMC free article] [PubMed]