We estimate that more than half of the excess distal gastric cancer incidence in Māori men and more than two thirds of that in Pacific men in New Zealand can be explained by H. pylori infection. Several factors have been proposed as contributors to the excess burden of gastric cancer in indigenous populations [1, 11], including poor nutrition and sanitation, excess salt, inadequate fruit and vegetable intake, and genetic predisposition. Our findings suggest that H. pylori infection explains most of the association, although the other factors mentioned may interact with or share a common causal pathway with H. pylori. It is likely that these findings can be generalized to Māori and Pacific women and to other indigenous and ethnic groups with high H. pylori prevalence and high gastric cancer incidence rates.
This report is one of the first to quantify the contribution of H. pylori to ethnic inequalities in gastric cancer incidence. Our results, however, may have been underestimated because of nondifferential measurement bias relating to H. pylori infection. The serology test does not distinguish the length of exposure to chronic infection, the intensity of infection, or the malignant potential of the subtype of H. pylori acquired. H. pylori seronegativity may be associated with severe atrophic gastritis or intestinal metaplasia caused by H. pylori infection; and thus the high risk of gastric cancer with these mucosal changes may also result in a slight underestimation of the impact of H. pylori on gastric cancer . It is possible too that H. pylori infection is correlated with confounders such as smoking. However, we think this alternative hypothesis is unlikely. For example, our sensitivity analysis for “residual mediation” by smoking explained little more of the ethnic difference. We assumed that all distal cancers occur in people who have H. pylori infection. This assumption may have inflated our results slightly; however, it is the best estimate of H. pylori contribution we could calculate given the evidence available, and in our view is likely to be more than offset by possible nondifferential misclassification of H. pylori status. Our findings were robust in relation to the sensitivity analyses we performed (see the electronic supplementary material).
H. pylori is likely to be the major contributor to excess Māori and Pacific gastric cancer incidence. Pro-equity interventions should be developed to reduce the prevalence of H. pylori infection, particularly in high-risk groups. This includes measures that address overcrowding and acquisition of infection [13, 14], and H. pylori eradication strategies, particularly if stronger evidence is produced that shows the benefits from screening outweigh any harms [15, 16].