Editor—In their editorial, Jankowski et al provide useful information on molecular changes leading to adenocarcinoma of the oesophagus and gastro-oesophageal junction.1 The incidence of and mortality from oesophageal adenocarcinoma have risen dramatically over the past few decades in Europe and North America. One very important explanation for the rise in incidence is the increase in overweight.
A case-control study in British women confirmed the findings of at least four previous studies in reporting a significant positive association between overweight and oesophageal adenocarcinoma.2 A further epidemiological study has shown a highly significant association between reflux symptoms and oesophageal adenocarcinoma.3 It is now 50 years since we first identified a link between tobacco smoking and many chronic diseases. Since then, the simple avoidance of tobacco products has prevented millions of premature deaths, in contrast to the limited role of improved understanding of molecular biology. We doubt that things would be much different in the near future, notwithstanding the promise of the human genome project. Although the work reviewed by Jankowski et al is of potential importance for screening or treatment, as well as increasing our knowledge on oesophageal carcinogenesis, we must not lose sight of the importance of lifestyle changes that would lower the risk of this cancer by reducing the population prevalence of overweight. In the context of the United Kingdom this is especially important, given that our oesophageal adenocarcinoma rates are the highest in Europe and among the highest in the world.4
References
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