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Vitamins B₂, B₆, and B₁₂ and Risk of New Colorectal Adenomas in a Randomized Trial of Aspirin Use and Folic Acid Supplementation

¹ Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California; ² Departments of Community and Family Medicine, Dartmouth Medical School, Hanover, New Hampshire; ³ Bevital A/S, Armauer Hansens Hus; ⁴ Section for Pharmacology, Institute of Medicine, University of Bergen and Haukeland University Hospital, Bergen, Norway; ⁵ Department of Medicine, University of Colorado, Denver, Colorado; ⁶ Laboratory of Molecular Technology, SAIC-Frederick, Inc., Frederick, Maryland; ⁷ Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland; and ⁸ Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, New Hampshire

Requests for reprints: Jane C. Figueiredo, Department of Preventive Medicine, University of Southern California, Harlyne J Norris Cancer Research Tower, 1450 Biggy Street Room 1509B, Los Angeles CA 90033. Phone: 323-442-7752; Fax: 323-442-7787. E-mail: janefigu{at}usc.edu

Background: Folate, other vitamin B cofactors, and genes involved in folate-mediated one-carbon metabolism all may play important roles in colorectal neoplasia. In this study, we examined the associations between dietary and circulating plasma levels of vitamins B₂, B₆, and B₁₂ and risk colorectal adenomas.

Methods: The Aspirin/Folate Polyp Prevention Study is a randomized clinical trial of folic acid supplementation and incidence of new colorectal adenomas in individuals with a history of adenomas (n = 1,084). Diet and supplement use were ascertained through a food frequency questionnaire administered at baseline. Blood collected at baseline was used to determine plasma B-vitamin levels. We used generalized linear regression to estimate risk ratios (RR) and 95% confidence intervals (95% CI) as measures of association.

Results: We found a borderline significant inverse association with plasma B₆ [pyridoxal 5'-phosphate (PLP)] and adenoma risk (adjusted RR Q4 versus Q1, 0.78; 95% CI, 0.61-1.00; P_trend = 0.08). This association was not modified by folic acid supplementation or plasma folate. However, the protective association of PLP with adenoma risk was observed only among subjects who did not drink alcohol (P_interaction = 0.03). Plasma B₂ (riboflavin) was inversely associated with risk of advanced lesions (adjusted RR Q4 versus Q1, 0.51; 95% CI, 0.26-0.99; P_trend = 0.12). No significant associations were observed between adenoma risk and plasma vitamin B₁₂ or dietary intake of vitamin B₂ and B₆. When we examined specific gene-B-vitamin interactions, we observed a possible interaction between methylenetetrahydrofolate reductase -C677T and plasma B₂ on risk of all adenomas.

Conclusion: Our results suggest that high levels of PLP and B₂ may protect against colorectal adenomas. (Cancer Epidemiol Biomarkers Prev 2008;17(8):2136–45)

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