Capsaicin consumption, Helicobacter pylori CagA status and IL1B-31C>T genotypes: A host and environment interaction in gastric cancer

• Published in: Food and chemical toxicology 2012-06, Vol.50 (6), p.2118-2122
• Main Authors: López-Carrillo, Lizbeth, Camargo, M. Constanza, Schneider, Barbara G., Sicinschi, Liviu A., Hernández-Ramírez, Raúl U., Correa, Pelayo, Cebrian, Mariano E.
• Format: Article
• Language: English
• Subjects: active ingredients; Adenocarcinoma - genetics; Adenocarcinoma - microbiology; Adult; Aged; alleles; Antibodies, Bacterial - analysis; at-risk population; Capsaicin; Capsaicin - adverse effects; Chili pepper; Diet; DNA; DNA - biosynthesis; DNA - genetics; environmental factors; enzyme-linked immunosorbent assay; Female; food frequency questionnaires; Gastric cancer; Gene-Environment Interaction; Genotype; Helicobacter Infections - complications; Helicobacter Infections - microbiology; Helicobacter pylori; Helicobacter pylori - drug effects; Helicobacter pylori - immunology; Helicobacter pylori CagA+; hot peppers; Humans; Immunoglobulin G - analysis; Interleukin 1 beta polymorphism; Interleukin-1beta - genetics; Logistic Models; Male; Mexico; Middle Aged; mortality; patients; Polymerase Chain Reaction; regression analysis; Risk; risk groups; sequence analysis; stomach neoplasms; Stomach Neoplasms - genetics; Stomach Neoplasms - microbiology; toxicology; virulence
• ISSN: 0278-6915; 1873-6351
• DOI: 10.1016/j.fct.2012.02.043

► Dietary, infectious and genetic factors interact to modulate gastric cancer (GC) risk. ► We explored chili pepper consumption, Helicobacter pylori infection and IL1B-31 genotypes. ► Capsaicin intake increased GC risk in IL1B-31C carriers infected with CagA+ H. pylori. ► Gene–environment interactions may explain GC incidence trends in Mexico. Gastric cancer (GC) has been associated with a complex combination of genetic and environmental factors. In contrast to most countries, available information on GC mortality trends showed a gradual increase in Mexico. Our aim was to explore potential interactions among dietary (chili pepper consumption), infectious (Helicobacter pylori) and genetic factors (IL1B-31 genotypes) on GC risk. The study was performed in three areas of Mexico, with different GC mortality rates. We included 158 GC patients and 317 clinical controls. Consumption of capsaicin (Cap), the pungent active substance of chili peppers, was estimated by food frequency questionnaire. H. pylori CagA status was assessed by ELISA, and IL1B-31 genotypes were determined by TaqMan assays and Pyrosequencing in DNA samples. Multivariate unconditional logistic regression was used to estimate potential interactions. Moderate to high Cap consumption synergistically increased GC risk in genetically susceptible individuals (IL1B-31C allele carriers) infected with the more virulent H. pylori (CagA+) strains. The combined presence of these factors might explain the absence of a decreasing trend for GC in Mexico. However, further research on gene–environment interactions is required to fully understand the factors determining GC patterns in susceptible populations, with the aim of recommending preventive measures for high risk individuals.