Background: In the Western world, the incidence of oesophageal adenocarcinoma has increased over the last 30 years coinciding with a decrease in the prevalence of Helicobacter pylori. Trends of increasing oesophageal adenocarcinoma can be linked causally to increasing gastro-oesophageal reflux disease (GORD) which can be linked to an increasingly obese population. However, there is no plausible biological mechanism of association between H pylori, obesity, and GORD. Ghrelin, a peptide produced in the stomach, which regulates appetite, food intake, and body composition, was studied in H pylori positive asymptomatic subjects.

Methods: Plasma ghrelin, leptin, and gastrin were measured for six hours after an overnight fast, before and after cure of H pylori in 10 subjects. Twenty four hour intragastric acidity was also assessed.

Results: After cure, median (95% confidence intervals) integrated plasma ghrelin increased from 1160.5 (765.5–1451) pg/ml×h to 1910.4 (1675.6–2395.6) pg/ml×h (p=0.002, Wilcoxon’s rank sum test), a 75% increase. This was associated with a 14% increase in 24 hour intragastric acidity (p=0.006) and non-significant changes in leptin and gastrin. There was a significant positive correlation between plasma ghrelin and intragastric acidity (r_s 0.44, p=0.05, Spearman’s rank correlation)

Conclusions: After H pylori cure, plasma ghrelin increased profoundly in asymptomatic subjects. This could lead to increased appetite and weight gain, and contribute to the increasing obesity seen in Western populations where H pylori prevalence is low. This plausible biological mechanism links H pylori, through increasing obesity and GORD, to the increase in oesophageal adenocarcinoma observed in the West.