TY - JOUR
T1 - Intakes of Dietary Folate and Other B Vitamins Are Associated with Risks of Esophageal Adenocarcinoma, Barrett's Esophagus, and Reflux Esophagitis
AU - Sharp, Linda
AU - Carsin, Anne-Elie
AU - Cantwell, Marie M.
AU - Anderson, Lesley A.
AU - Murray, Liam J.
AU - FINBAR Study Group
N1 - Acknowledgments
The authors thank Siobhan Reynolds, Majella Gallagher, Carol Anderson, and Martin McAnaespie for subject recruitment, Damian McManus for help with classifying the tumor sites, and Helen Mulholland for helpful comments on an earlier draft of the manuscript. The FINBAR study group members are L.J. Murray, L.A. Anderson (Queen's University Belfast); B.T. Johnston, R.G.P. Watson, J. McGuigan, H.R. Ferguson (Belfast Health and Social Care Trust, Belfast, Country Antrim, UK); S.J. Murphy (St Vincent's Hospital, Dublin, Ireland); J.V. Reynolds (St James' Hospital, Dublin, Ireland); and H. Comber (National Cancer Registry Ireland). L.J.M. and L.A.A. designed the FINBAR study; L.A.A. conducted the study; L.J.M. supervised the study; M.M.C. provided dietary assessment expertise; L.S. had the idea for this analysis; A.-E.C. and L.S. analyzed data; and L.S. wrote the paper and has primary responsibility for final content. All authors read and approved the final manuscript.
Supported by a Ireland-Northern Ireland Co-operation Research Project Grant sponsored by the Research and Development Office, Belfast and the Health Research Board Dublin, and by the Ulster Cancer Foundation, Northern Ireland. The reflux esophagitis data collection was supported by a Research and Development Office Clinical Fellowship.
PY - 2013/12/1
Y1 - 2013/12/1
N2 - Folate is implicated in carcinogenesis via effects on DNA synthesis, repair, and methylation. Efficient folate metabolism requires other B vitamins and is adversely affected by smoking and alcohol. Esophageal adenocarcinoma (EAC) may develop through a process involving inflammation [reflux esophagitis (RE)] leading to metaplasia [Barretts esophagus (BE)] and carcinoma. Within a population-based, case-control study, we investigated associations between dietary folate and related factors and risks of EAC, BE, and RE. EAC and BE cases had histologically confirmed disease; RE cases had endoscopically visible inflammation. Controls, age-sex frequency matched to EAC cases, were selected through population and general practice registers. Participants underwent structured interviews and completed food-frequency questionnaires. Multivariate ORs and 95% CIs were computed using logistic regression. A total of 256 controls and 223 EAC, 220 BE, and 219 RE cases participated. EAC risk decreased with increasing folate intake (OR highest vs. lowest = 0.56; 95% CI: 0.31, 1.00; P-trend < 0.01). Similar trends were found for BE (P-trend < 0.01) and RE (P-trend = 0.01). Vitamin B-6 intake was significantly inversely related to risks of all 3 lesions. Riboflavin intake was inversely associated with RE. Vitamin B-12 intake was positively associated with EAC. For EAC, there was a borderline significant interaction between folate intake and smoking (P-interaction = 0.053); compared with nonsmokers with high (≥median) folate intake, current smokers with low intakes (
AB - Folate is implicated in carcinogenesis via effects on DNA synthesis, repair, and methylation. Efficient folate metabolism requires other B vitamins and is adversely affected by smoking and alcohol. Esophageal adenocarcinoma (EAC) may develop through a process involving inflammation [reflux esophagitis (RE)] leading to metaplasia [Barretts esophagus (BE)] and carcinoma. Within a population-based, case-control study, we investigated associations between dietary folate and related factors and risks of EAC, BE, and RE. EAC and BE cases had histologically confirmed disease; RE cases had endoscopically visible inflammation. Controls, age-sex frequency matched to EAC cases, were selected through population and general practice registers. Participants underwent structured interviews and completed food-frequency questionnaires. Multivariate ORs and 95% CIs were computed using logistic regression. A total of 256 controls and 223 EAC, 220 BE, and 219 RE cases participated. EAC risk decreased with increasing folate intake (OR highest vs. lowest = 0.56; 95% CI: 0.31, 1.00; P-trend < 0.01). Similar trends were found for BE (P-trend < 0.01) and RE (P-trend = 0.01). Vitamin B-6 intake was significantly inversely related to risks of all 3 lesions. Riboflavin intake was inversely associated with RE. Vitamin B-12 intake was positively associated with EAC. For EAC, there was a borderline significant interaction between folate intake and smoking (P-interaction = 0.053); compared with nonsmokers with high (≥median) folate intake, current smokers with low intakes (
UR - http://www.scopus.com/inward/record.url?scp=84888412086&partnerID=8YFLogxK
U2 - 10.3945/jn.113.174664
DO - 10.3945/jn.113.174664
M3 - Article
C2 - 24132576
AN - SCOPUS:84888412086
VL - 143
SP - 1966
EP - 1973
JO - The Journal of Nutrition
JF - The Journal of Nutrition
SN - 0022-3166
IS - 12
ER -