Barrett’s oesophagus and oesophageal adenocarcinoma are on the increase [1]. In fact, adenocarcinoma of the oesophagus is the tumour with the fastest growing incidence in the Western world [2]. The relative proportion of squamous and adenocarcinoma has completely reversed in many parts of the world, the increase in the latter mirroring the vast and rapid increase in the incidence of gastro-oesophageal reflux disease (GORD) and Barrett’s oesophagus. Indeed, within the Asian population significant differences are seen [3]. In Singapore, there has been a large increase in the number of cases of oesophageal adenocarcinoma and a relative decrease in the incidence of squamous carcinoma of the oesophagus [4]. In Japan, on the other hand, the incidence of both cancers remains relatively unchanged.

The reason for this rapid increase is unknown, and many hypotheses have been put forward to explain it [5]. It is unknown whether these changes are genetic in nature, environmental or a mixture of the two. There are also significant inter-racial differences in the incidence of Barrett’s oesophagus and oesophageal adenocarcinoma. Again it is unknown whether these differences are because of genetic or environmental factors, or indeed a mixture of the two. In this article, Dr Rajendra addresses this issue in a very comprehensive and compelling manner.

The South East Asian population is an ideal population in which to study these differences as there are distinct racial/genetic groups living in close proximity. This article looks at the various known genetic and environmental risk factors for Barrett’s oesophagus and oesophageal adenocarcinoma in an attempt to answer the question of whether ethnic differences are because of genetic and/or environmental factors. Dr Rajendra presents all the evidence and considers each aetiological factor in turn.

Ethnic differences in GORD and Barrett’s oesophagus are well described in Asian populations [6]. Twin and family studies suggest a genetic component to GORD; also, familial aggregation of GORD symptoms is well documented [7]. There is a known increase in Barrett’s oesophagus and oesophageal adenocarcinoma in Caucasian patients with GORD [8], but no similar studies have been reported in the Asian population.

The author outlines the racial differences in the incidence of Barrett’s oesophagus across the world. Middle Eastern populations have a much higher incidence than those in the Far East. In both the UK and USA, studies have shown a higher incidence in White people as compared to Black people [9]. In the multi-racial Malaysian population, the incidence of Barrett’s oesophagus is significantly higher in the Indians than in the Malays and Chinese. Equally, twin studies in both Sweden and the UK show a positive correlation as compared to controls, with an increased concordance in monozygotic twins (approximately 40%) as compared to dizygotic twins (around 30%)[10]. All of these studies suggest a genetic aetiological factor but there have been no reported Asian twin studies.

Dr Rajendra presents us with a list of positive and negative aetiological factors for Barrett’s oesophagus and then goes on to deal with the specifics of each one in turn. The factors listed as having a positive correlation with Barrett’s oesophagus are hiatus hernia, chronic GORD, male sex, Caucasian and Indian races, HLA-B07 gene, obesity, metabolic syndrome, smoking and Western diet. The negative (protective) factors include Helicobacter pylori infection and increased fruit and vegetable intake.

In Asian populations, there has traditionally been a much higher incidence of H. pylori infection than in the West, thus affording relative protection against GORD and Barrett’s oesophagus but with increasing ‘Westernisation’H. pylori infection is reducing and GORD/Barrett’s is on the increase. Indeed there are differences within the Asian population, with H. pylori being more common in Indians than Chinese and even less common in Malays [11]. However, there is a paradoxical increased incidence of GORD in the Indian population. This may be more related to increased genetic predisposition because of the HLA-B07 gene, which is more common in both Caucasian and Indian races.

There is an inverse relationship between H. pylori infection and both oesophagitis and Barrett’s oesophagus. Indeed there is an inverse correlation between H. pylori infection and the length of Barrett’s oesophagus, the longer the segment of columnar lined oesophagus, the less likelihood of H. pylori infection [12].

Obesity is discussed as a risk factor for GORD/Barrett’s/adenocarcinoma, with an increased risk with increasing body mass index. This is almost certainly because of the increase in gastro-oesophageal reflux with increasing weight, especially abdominal girth. It is, however, pointed out that this is only really true in White people and not so much in the Asian and Black populations [13].

Hiatus hernia is presented as a risk factor, the mechanism in this case being easy to understand, with the hernia leading to GORD and subsequent metaplastic/dysplastic/neoplastic changes. There are regional variations in the relationship between hiatus hernia and Barrett’s oesophagus but the pattern is essentially the same the world over. In the West, over 90% of patients with Barrett’s oesophagus have an associated hiatus hernia. In Japan, over 70% of patients over the age of 70 years with Barrett’s have a hiatus hernia [14].

Smoking is presented as a possible risk factor for metaplastic changes and subsequent oesophageal adenocarcinoma but, unlike with squamous cell carcinoma of the oesophagus, there is no conclusive evidence for this relationship [15].

Dietary factors are discussed. The author points out that most of know anecdotally that curries and spicy foods lead to reflux and so these may be an aetiological factor. On the other hand, it appears that a diet rich in fruit and vegetables may be protective against reflux and the associated conditions [16].

Dr Rajendra concludes by stating that the increased incidence of Barrett’s oesophagus is probably a combination of a true increased incidence, together with an increased diagnosis owing to greater awareness of the condition and the use of better endoscopy equipment. He postulates that the main factors behind this increased incidence are a combination of various environmental factors, including GORD, obesity, Western diet and a decreasing incidence of H. pylori infection.

Having read this article with interest, I am still not sure whether we can answer the question as to whether ethnic differences in Barrett’s oesophagus in the Asian population are because of genes or the environment and I feel sure that it will turn out to be owing to a combination of the two. However, this paper certainly makes for entertaining reading and provides food for thought as to the aetiology of Barrett’s oesophagus and oesophageal adenocarcinoma in both the South East Asian population and across the world in general. Dr Rajendra is to be congratulated on his review of this disease and its aetiology.

Conflict of interest statement

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  2. Conflict of interest statement
  3. References

No conflicts of interest to declare.


  1. Top of page
  2. Conflict of interest statement
  3. References