Copyright ©The Author(s) 1999. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Feb 15, 1999; 5(1): 4-6
Published online Feb 15, 1999. doi: 10.3748/wjg.v5.i1.4
Gastroesophageal reflux disease is uncommon in Asia: evidence and possible explanations
Khek-Yu Ho
Khek-Yu Ho, Department of Medicine, National University of Singapore, Singapore 119260, Singapore
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr Khek-Yu Ho, MBBS (Syd Hons 1) FRACP FAMS, Department of Medicine, National University Hospital, Low-er Kent Ridge Road, Singapore 119074. mdchoky@nus.edu.sg
Telephone: +65-7724353 Fax: +65-7794112
Received: December 30, 1998
Revised: January 22, 1999
Accepted: January 29, 1999
Published online: February 15, 1999

Key Words: gastroesophageal reflux, esophagitis, Barrett’s esophagus, hiatus hernia, Helicobacter pylori, gastric acid


Gastroesophageal reflux that predisposes an indivi-dual to the risk of physical complications, or produces symptoms leading to significantly impaired quality of life, is termed gastroesophageal reflux disease (GERD)[1]. Clinically, GERD encompasses a broad spectrum of separate, though related condi-tions that are sometimes conveniently grouped under two broad categories: endoscopic esophag itis and endoscopy negative reflux disease. Endoscopic esophagitis is considered to be present when there is endoscopically visible breakage of the mucosa[2], re-gardless of whether the patient has symptoms. The term “endoscopic negative reflux disease” refers to GERD that is not associated with Barrett’s esopha-gus or esophageal mucosal breaks. It includes such conditions as esoph ageal mucosal acid sensitivity, which is symptomatic reflux induced by acid reflux and proven by objective means; abnormal esophageal acid exposure, which is excessive acid reflux confirmed by objective measures; and reflux-type symptoms (heartburn and/or acid regurgitation) that clearly dominate the patient’s com-plaints[3]. Barrett’s esophagus is the eponym applied to the columnar epithelium-lined lower esophagus that is acquired as a consequence of chronic gas troe-sophageal reflux[4]. Hiatus hernia, on the other hand, has been defined as a displacement of the gas-tric mucosa 1.5 cm or more above the diaph ragmatic hiatus[5].

Prevalence of reflux-type symptoms in general population

Until recently, there has been no systematic study on the prevalence of reflux type symptoms in the general population of Asia. A cross-sectional survey of a race-stratified sample of adults in a Singaporean town provides some of the first evidences, that re-flux-type symptoms are uncommon in the East[6]. Of 696 persons evaluated, only 2% had heartburn and/ or acid regurgitation for more than once a month. This prevalence is much lower than those (29%-44%) of Wester n populations[7,8].

Prevalence of GERD in pregnant women

The individuals with the highest prevalence of heartburn are often said to be pregnant women. A prospective study, using a reliable questionnaire, on a consecutive series of pregnant women in Singapore, provides the second piece of evidence that reflux-type symptoms are uncommon among Asians[9]. Of the 35 pregnant women evaluated, 23% had heartburn some time during their pregnancy. This percentage is lower than those (48%-96%)reported previously in the West[10,11].

Frequency of GERD in outpatient clinics

In a large clinical series from Singapore, Kang et al from Singapore noted a 2% frequency of GERD among 2141 consecutive patients investigated[12]. The diagnosis of GERD was established on the basis of an abnormal endoscopy, a positive acid perfusion test and/or an abnormal 24-hour pH monitoring. The frequency was lower as compared with a similar series from the West[13].

Prevalence of endoscopic esophagitis

Very few epidemiological data on reflux esophagitis in Asians are available in the literature. However, Chang et al found 5% with reflux esophagitis[14] in an endoscopic series of 2044 patients who underwent self-paid medical check-ups. Esophagitis, when present, was often mild. The prevalence of endoscopic esophagitis among symptomatic subjects has not been well studied and the available data are conflicting. In a study from Taiwan, a 15% prevalence of erosive esophagitis was found in 455 consecutive patients evaluated for various upper gastrointestinal tract symptoms[15]. Most of the patients presented with mild esophagitis. The expected high frequency of erosive esophagitis is not supported by other en-doscopic series from Asia. Erosive esophagitis was uncommon in both indigenous Fijians and Indians, being detected in only 2% of a total of 693 endo-scopic examinations[16]. This contrasts with the higher prevalence (11%) of reflux esophagitis noted by the same author among New Zealanders[17]. Esophagitis is likewise uncommon in Japan; a preva-lence rate of 3% was recorded among 240 consecu-tive outpatients with dyspepsia[18]. Our own retro-spective series from Singapore showed that of 11943 patients undergoing diagnostic upper endoscopy for various complaints, 4% had esophagitis[19]. This frequency was lower than those reported from West-ern centers[20,21]. Thus, with the exception of the Taiwanese series, the proportion of patients with endoscopic esophagitis in Asian series appears lower than that in reports from Western countries. The severity of esophagitis also appears mild, unlike that in Western populations[20,21].

Prevalence of hiatus hernia

Hiatus hernia, as seen on barium studies, appears rare in the Far East with a < 1% prevalence[22]. Recent endoscopic series from Asia confirm this im-pression. Chang et al from Taiwan found hiatus hernia in 2% of patients endoscoped as part of an annual medical examination[14]. In another Tai-wanese study in patients endoscoped for gastroin-testinal complaints, hiatus hernia was found in 7% of the cases[15]. In our retrospective series from Sin-gapore, the proportion of hiatus hernia among pa-tients seen for gastrointestinal complaints was 3%[19]. Thus, the available data show that the prevalence of hiatus hernia is lower than that in Western series (17%-22%)[20,21].

Prevalence of GERD complications

The prevalence of Barrett’s esophagus varies, de-pending on the population being studied. In a series from Taiwan, 2% of patients endoscoped for a variety of upper gastrointestinal symptoms were found to have Barrett’s esophagus[15]. When evaluating only those with erosive esophagitis, this rate in-creased to 14%. The corresponding figures from the West are 4%-20%[23,24] and 36%, respectively[23]. Reports from a Taiwanese center, and our own cen-ter showed a frequency of benign (presumably reflux-related) esophageal stricture of only 0.4% and 0.2% respectively, among patients endoscoped for various gastrointestinal indications[16,19]. These fre-quencies are lower in comparison with those in reports from the West[25].


The pathogenesis of reflux esophagitis can be considered in terms of excessive acid load overwhelming mucosal defense. The degree of acid load is in turn determined by the anti-reflux barrier of the gastro-esophageal junction[26], the quantity of acid re-fluxed[27], and the ability of the esophagus to clear any refluxate back into the stomach[28]. The latter depends on the integrity of peristaltic function[29] and the neutralizing ability of swallowed saliva[28]. More recently, an inverse relationship between He-licobacter pylori (H. pylori) and GERD has been suggested[30]. By examining the potential patho-genetic factors, it is hoped that the lower frequency of GERD in the East than in the West could be explained.

Anti-reflux barrier

An increase in intra-abdominal and intragastric pressure overcomes the gastroes ophageal pressure gradient maintained by the lower esophageal sphinc-ter (LES). Such an increase may occur through obesity[31] and delayed gastric emptying by fatty meals[32]. Alcohol, smoking and fat can lower the LES pressure and esophageal peristalsis, thus favor-ing the occurrence of gastroesophageal reflux[33-35]. A large hiatus hernia traps gastric contents in its pouch above the diaphragm. This leads to free retrograde flow of acid into the esopha gus.

Increased body mass index and presence of hiatus hernia were found to be the most important factors associated with the occurrence of esophagitis in a recent study from Taiwan[14]. The authors suggested that the lower prevalence of hiatus hernia and smaller body mass index in the Chinese population might account for the lower prevalence of reflux esophagitis in Taiwan. The low prevalence of hiatus hernia in the East has previously been attributed to the consumption of high residue diets in the developing world[22]. Another report from Tai-wan found erosive esophagitis to be associated with smoking, and alcohol consumption[15]. The authors suggested that the recent increase in smoking, alcohol use, and fat consumption among Taiwanese were contributed to the observed rise in the preva-lence of GERD in Taiwan.

Gastric acid output

Since acid secretion correlates with body surface area, Asians in general are characterized by a smaller parietal cell mass and a lower acid output as com-pared with Caucasians[36]. Except for the striking example of Zollinger-Ellis on syndrome, however, the association between the amount of acid output and the occurrence or severity of reflux disease has remained unproven[37].

Acid clearance

While evaluating the consecutive Singaporean pa-tients who underwent esophageal manometry, we found that poor esophageal clearnance was more common among those with esophagitis than among those without. The results were identical to Western studies[38]. It is possible that this clearance mecha-nism has an inherited basis, and is more efficient in Asians than in Caucasians. Data to support this is, however, lacking.

Mucosal defence

Presently, there is no risk factor known to disrupt tissue resistance, except for nonsteroidal anti-in-flammatory drugs[39]. Such drugs cannot be an im-portant factor underlying the geographical variation in the prevalence of GERD, because they are consumed by Asians no more than by Westerners. How-ever, it is possible that inborn differences in tissue resistance, due to yet unrecognized factors, may ac-count for some of the geographical differences.

H. pylori infection

There is circumstantial evidence to suggest that H. pylori infection is rela tively protective for the oc-currence of GERD[30]. It has been suggested that Hong Kong Chinese are protected against reflux esophagitis by their high prevalence of H. pylori associated gastritis[40]. Such gastritis, when beco-ming chronic, can lead to gastric atrophy and hypochlorhydria, thereby reducing the likelihood of GERD. If this hypothesis is correct, the effects of H. pylori induced gastritis may be an important factor determining the lower prevalence of reflux esophagitis in this part of the world, in which H. pylori infection is especially common. No data, however, exists to support this hypot hesis.

Genetic factors

It is unlikely that the lower frequency of GERD in Asian populations can be explained simply by the known extrinsic risk factors, such as obesity, smo-king habits, and alcohol consumption, being less frequent in Asians as compared with Caucasians. It is likely that genetic factors are involved. If that was the case, the mechanisms through which they confer protection against GERD are poorly understood. It may be that LES function is truly more competent in Asians compared with Westerners. Alternatively, the esophageal mucosa in Asians is in-herently more acid resistant. Differences in gastric acid output and esophageal clearance ability between Asian and Western patients are further possi-bilities. Comparative studies into these parameters in Eastern and Western populations may shed more light on this question, and may lead to formulation of appropriate- therapeutic strategies.

In summary, most reports from Asia have sug-gested that GERD is an uncommon condition in this part of the world. The reasons for the lower fre-quency compared with the West are not known, and further studies are required.


Edited by Jing-Yun Ma

1.  Dent J, Brun J, Fredrick AM, Fennerty MB, Janssens J, Kahrilas PJ. An evidence-based appraisal of reflux disease management--the Genval Workshop Report. Gut. 1999;44 Suppl 2:S1-16.  [PubMed]  [DOI]
2.  Armstrong D, Bennett JR, Blum AL, Dent J, De Dombal FT, Galmiche JP, Lundell L, Margulies M, Richter JE, Spechler SJ. The endoscopic assessment of esophagitis: a progress report on observer agreement. Gastroenterology. 1996;111:85-92.  [PubMed]  [DOI]
3.  Klauser AG, Schindlbeck NE, Müller-Lissner SA. Symptoms in gastro-oesophageal reflux disease. Lancet. 1990;335:205-208.  [PubMed]  [DOI]
4.  Cameron AJ. Epidemiology of columnar-lined esophagus and adenocarcinoma. Gastroenterol Clin North Am. 1997;26:487-494.  [PubMed]  [DOI]
5.  Pridie RB. Incidence and coincidence of hiatus hernia. Gut. 1966;7:188-189.  [PubMed]  [DOI]
6.  Ho KY, Kang JY, Seow A. Prevalence of gastrointestinal symptoms in a multiracial Asian population, with particular reference to reflux-type symptoms. Am J Gastroenterol. 1998;93:1816-1822.  [PubMed]  [DOI]
7.  Locke GR, Talley NJ, Fett SL, Zinsmeister AR, Melton LJ. Prevalence and clinical spectrum of gastroesophageal reflux: a population-based study in Olmsted County, Minnesota. Gastroenterology. 1997;112:1448-1456.  [PubMed]  [DOI]
8.  Drossman DA, Li Z, Andruzzi E, Temple RD, Talley NJ, Thompson WG, Whitehead WE, Janssens J, Funch-Jensen P, Corazziari E. U.S. householder survey of functional gastrointestinal disorders. Prevalence, sociodemography, and health impact. Dig Dis Sci. 1993;38:1569-1580.  [PubMed]  [DOI]
9.  Ho KY, Kang JY, Viegas OA. Symptomatic gastro-oesophageal reflux in pregnancy: a prospective study among Singaporean women. J Gastroenterol Hepatol. 1998;13:1020-1026.  [PubMed]  [DOI]
10.  NAGLER R, SPIRO HM. Heartburn in pregnancy. Am J Dig Dis. 1962;7:648-655.  [PubMed]  [DOI]
11.  Bainbridge ET, Temple JG, Nicholas SP, Newton JR, Boriah V. Symptomatic gastro-oesophageal reflux in pregnancy. A comparative study of white Europeans and Asians in Birmingham. Br J Clin Pract. 1983;37:53-57.  [PubMed]  [DOI]
12.  Kang JY, Yap I, Gwee KA. The pattern of functional and organic disorders in an Asian gastroenterological clinic. J Gastroenterol Hepatol. 1994;9:124-127.  [PubMed]  [DOI]
13.  Harvey RF, Salih SY, Read AE. Organic and functional disorders in 2000 gastroenterology outpatients. Lancet. 1983;1:632-634.  [PubMed]  [DOI]
14.  Chang CS, Poon SK, Lien HC, Chen GH. The incidence of reflux esophagitis among the Chinese. Am J Gastroenterol. 1997;92:668-671.  [PubMed]  [DOI]
15.  Yeh C, Hsu CT, Ho AS, Sampliner RE, Fass R. Erosive esophagitis and Barrett's esophagus in Taiwan: a higher frequency than expected. Dig Dis Sci. 1997;42:702-706.  [PubMed]  [DOI]
16.  Scobie BA, Beg F, Oldmeadows M. Peptic diseases compared endoscopically in indigenous Fijians and Indians. N Z Med J. 1987;100:683-684.  [PubMed]  [DOI]
17.  Scobie BA. Endoscopy in peptic diseases and bleeding: a community survey of 1635 patients. N Z Med J. 1988;101:78-80.  [PubMed]  [DOI]
18.  Inoue M, Sekiguchi T, Harasawa S, Miwa T, Miyoshi A. Dyspepsia and dyspepsia subgroups in Japan: symptom profiles and experience with cisapride. Scand J Gastroenterol Suppl. 1993;195:36-38; discussion 38-39.  [PubMed]  [DOI]
19.  Kang JY, Tay HH, Yap I, Guan R, Lim KP, Math MV. Low frequency of endoscopic esophagitis in Asian patients. J Clin Gastroenterol. 1993;16:70-73.  [PubMed]  [DOI]
20.  Berstad A, Weberg R, Frøyshov Larsen I, Hoel B, Hauer-Jensen M. Relationship of hiatus hernia to reflux oesophagitis. A prospective study of coincidence, using endoscopy. Scand J Gastroenterol. 1986;21:55-58.  [PubMed]  [DOI]
21.  Wright RA, Hurwitz AL. Relationship of hiatal hernia to endoscopically proved reflux esophagitis. Dig Dis Sci. 1979;24:311-313.  [PubMed]  [DOI]
22.  Burkitt DP, James PA. Low-residue diets and hiatus hernia. Lancet. 1973;2:128-130.  [PubMed]  [DOI]
23.  Winters C, Spurling TJ, Chobanian SJ, Curtis DJ, Esposito RL, Hacker JF, Johnson DA, Cruess DF, Cotelingam JD, Gurney MS. Barrett's esophagus. A prevalent, occult complication of gastroesophageal reflux disease. Gastroenterology. 1987;92:118-124.  [PubMed]  [DOI]
24.  Mann NS, Tsai MF, Nair PK. Barrett's esophagus in patients with symptomatic reflux esophagitis. Am J Gastroenterol. 1989;84:1494-1496.  [PubMed]  [DOI]
25.  Sonnenberg A. Epidemiologie und Spontanverlauf der Refluxkrankheit. In Blum AL,Siewert JR, eds. Refluxtherapie. Gastroesophageale refluxkrankheit: konservative and operative therapie. Berlin: Springer Verlag. 1981;85-106.  [PubMed]  [DOI]
26.  Dodds WJ, Dent J, Hogan WJ, Helm JF, Hauser R, Patel GK, Egide MS. Mechanisms of gastroesophageal reflux in patients with reflux esophagitis. N Engl J Med. 1982;307:1547-1552.  [PubMed]  [DOI]
27.  Boesby S. Relationship between gastro-oesophageal acid reflux, basal gastro-oesophageal sphincter pressure, and gastric acid secretion. Scand J Gastroenterol. 1977;12:547-551.  [PubMed]  [DOI]
28.  Helm JF, Dodds WJ, Pelc LR, Palmer DW, Hogan WJ, Teeter BC. Effect of esophageal emptying and saliva on clearance of acid from the esophagus. N Engl J Med. 1984;310:284-288.  [PubMed]  [DOI]
29.  Kahrilas PJ, Dodds WJ, Hogan WJ. Effect of peristaltic dysfunction on esophageal volume clearance. Gastroenterology. 1988;94:73-80.  [PubMed]  [DOI]
30.  Labenz J, Blum AL, Bayerdörffer E, Meining A, Stolte M, Börsch G. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology. 1997;112:1442-1447.  [PubMed]  [DOI]
31.  Stene-Larsen G, Weberg R, Frøyshov Larsen I, Bjørtuft O, Hoel B, Berstad A. Relationship of overweight to hiatus hernia and reflux oesophagitis. Scand J Gastroenterol. 1988;23:427-432.  [PubMed]  [DOI]
32.  McCallum RW, Berkowitz DM, Lerner E. Gastric emptying in patients with gastroesophageal reflux. Gastroenterology. 1981;80:285-291.  [PubMed]  [DOI]
33.  Hogan WJ, Viegas de Andrade SR, Winship DH. Ethanol-induced acute esophageal motor dysfunction. J Appl Physiol. 1972;32:755-760.  [PubMed]  [DOI]
34.  Dennish GW, Castell DO. Inhibitory effect of smoking on the lower esophageal sphincter. N Engl J Med. 1971;284:1136-1137.  [PubMed]  [DOI]
35.  Nebel OT, Castell DO. Inhibition of the lower oesophageal sphincter by fat--a mechanism for fatty food intolerance. Gut. 1973;14:270-274.  [PubMed]  [DOI]
36.  Fung WP, Tye CY. Pentagastrin-stimulated gastric acid secretion in Chinese. Am J Gastroenterol. 1972;58:233-241.  [PubMed]  [DOI]
37.  Miller LS, Vinayek R, Frucht H, Gardner JD, Jensen RT, Maton PN. Reflux esophagitis in patients with Zollinger-Ellison syndrome. Gastroenterology. 1990;98:341-346.  [PubMed]  [DOI]
38.  Ho KY, Kang JY. Reflux esophagitis patients in Singapore have motor and acid exposure abnormalities similar to patients in the Western hemisphere. Am J Gastroenterol. 1999;94:1186-1191.  [PubMed]  [DOI]
39.  Lanas A, Hirschowitz BI. Significant role of aspirin use in patients with esophagitis. J Clin Gastroenterol. 1991;13:622-627.  [PubMed]  [DOI]
40.  Wu JCY, Go MYY, Chan WB, Choi CL, Chan FKL, Sung J. Prevalence and distribution of H. pylori in gastro- oesophageal reflux disease: a study in Chinese. Gastroenterology 114(4): A1364. .  [PubMed]  [DOI]