PT - JOURNAL ARTICLE AU - Steve Turner AU - Jon Ayres AU - Colin Palmer AU - Anil Mehta AU - Somnath Mukhopadhyay AU - Graham Devereux TI - Interactions between antioxidant gene variants and dietary antioxidant intake for asthma outcomes in children – Food for thought? DP - 2014 Sep 01 TA - European Respiratory Journal PG - P4244 VI - 44 IP - Suppl 58 4099 - http://erj.ersjournals.com/content/44/Suppl_58/P4244.short 4100 - http://erj.ersjournals.com/content/44/Suppl_58/P4244.full SO - Eur Respir J2014 Sep 01; 44 AB - Introduction. We tested the hypothesis that there is an interaction between reduced antioxidant dietary exposures and genetically determined susceptibility to oxidant stress for adverse asthma outcomes in children.Methods. Respiratory questionnaire, food frequency questionnaire (FFQ), Paediatric Asthma Quality of Life Questionnaire (PAQLQ) and Children's Asthma Control Test (CACT) were completed by children with asthma. Exposures of interest were energy-adjusted intake of vitamins C and E, carotenoids and selenium; a composite score (0 to 4) for antioxidant exposure was derived. DNA was extracted, GST variants were determined; a susceptibility score (0-3) for oxidant stress was derived. The primary outcome was a recent exacerbation and secondary outcomes were CACT and PAQLQ scores.Results. DNA and FFQ details were obtained in 450 children, mean age 10.3 years and 58% male. The risk for exacerbation, but not reduced CACT or PAQLQ scores, was concordant with increasing number of GST mutants (risk with no mutation 0.6 [95% CI 0.3, 0.9] compared to 2 or 3 mutations). There was no consistent association between individual antioxidant exposure or the dietary antioxidant exposure score and asthma outcomes. There was no interaction between reduced exposure to the dietary antioxidants measured and increased genetically determined antioxidant susceptibility for asthma exacerbation.Conclusion. Whilst our study was underpowered to detect an interaction of small magnitude, we found no evidence of a large effect of a gene-environment interaction between genetically-determined oxidant susceptibility and reduced dietary oxidant exposure for the outcomes.