Abstract A77: Gastric cancer risk in relation to capsaicin intake, H. pylori CagA status, and IL1B-31 C>T genotypes

Abstract

Abstract Background: In contrast to the situation in most countries, gastric cancer (GC) incidence is not declining in Mexico. Capsaicin (Cap) is the pungent active substance of chili peppers and it is related to an increased risk of GC in studies performed in Mexico, Spain, Serbia, Korea and India. Host genetic characteristics and variations in dietary patterns are considered concomitant risk factors for GC development. Helicobacter pylori (H. pylori) infection is considered a necessary but not sufficient cause of GC, as less than 3 % of infected patients develop this tumor. Increased risk for GC has been observed among Mexican C allele carriers of the pro-inflammatory interleukin 1B position-31 (IL1B-31) infected with more virulent H. pylori CagA = strains, we explored if that risk varies according to the consumption of Cap, since chili pepper consumption is highly prevalent among Mexicans. Methods: A total of 158 histologically confirmed GC patients and 317 clinical controls from three states with contrasting GC mortality rates in Mexico were included in this report. Cap intake was estimated by a previously validated food frequency questionnaire. H. pylori CagA status was assessed by an ELISA test, and genotypes of the IL1 B-31 were determined byTaqMan assays and Pyrosequencing in DNA samples isolated from serum. Results: Using unconditional adjusted logistic regression models, a significant 3.5-fold increased GC risk was observed among individuals with moderate to high Cap consumption, who were IL1B-31 C allele carriers and were H. pylori CagA positive, with a significant interaction term between Cap consumption and IL1B-31 genotypes (p=0.039): Odds Ratio (OR) among TC vs.TT carriers: 3.48; 95%CI: 1.01-12.0, and OR among CC vs. TT carriers: 3.37; 95%CI: 1.05-10.85; in contrast, no significant negative associations with GC were estimated when any of these three factors was absent. Conclusions. This is the first epidemiological report considering a potential interaction amongst dietary, infectious and genetic factors on GC risk and suggests that moderate to high Cap intake synergistically increases the risk of GC in genetically susceptible individuals (IL1 B-31 C allele carriers) infected with more virulent H. pylori (CagA positive) strains. The significant interaction between Cap consumption and genotypes of the IL1 B-31 suggests that a reduction of Cap intake under 30 mg/day among susceptible carriers with high consumption of Cap would reduce GC risk. Underlying mechanisms that explain these results, warrant attention and may include an up-regulation of H. pylori CagA expression in response to high capsaicin consumption. Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):A77.