Context Mounting evidence indicates that vitamin B6, a coenzyme involved in nearly 100 enzymatic reactions, may reduce the risk of colorectal cancer.
Objective To conduct a systematic review with meta-analysis of prospective studies assessing the association of vitamin B6 intake or blood levels of pyridoxal 5′-phosphate (PLP; the active form of vitamin B6) with risk of colorectal cancer.
Data Sources Relevant studies were identified by a search of MEDLINE and EMBASE databases to February 2010, with no restrictions. We also reviewed reference lists from retrieved articles.
Study Selection We included prospective studies that reported relative risk (RR) estimates with 95% confidence intervals (CIs) for the association between vitamin B6 intake or blood PLP levels and the risk of colorectal, colon, or rectal cancer.
Data Extraction Two authors independently extracted data and assessed study quality. Study-specific RRs were pooled using a random-effects model.
Data Synthesis Nine studies on vitamin B6 intake and 4 studies on blood PLP levels were included in the meta-analysis. The pooled RRs of colorectal cancer for the highest vs lowest category of vitamin B6 intake and blood PLP levels were 0.90 (95% CI, 0.75-1.07) and 0.52 (95% CI, 0.38-0.71), respectively. There was heterogeneity among studies of vitamin B6 intake (P = .01) but not among studies of blood PLP levels (P = .95). Omitting 1 study that contributed substantially to the heterogeneity among studies of vitamin B6 intake yielded a pooled RR of 0.80 (95% CI, 0.69-0.92). The risk of colorectal cancer decreased by 49% for every 100-pmol/mL increase (approximately 2 SDs) in blood PLP levels (RR, 0.51; 95% CI, 0.38-0.69).
Conclusion Vitamin B6 intake and blood PLP levels were inversely associated with the risk of colorectal cancer in this meta-analysis.
Pyridoxal 5′-phosphate (PLP), the principal active coenzyme form of vitamin B6, is involved in almost 100 enzymatic reactions.1 One function of vitamin B6 is its role in the 1-carbon metabolic pathway, which involves the transfer of 1-carbon groups for DNA synthesis and DNA methylation. Deficiency of vitamin B6 has been associated with considerably impaired 1-carbon metabolism in animals.2Hence, low vitamin B6 levels may increase colorectal cancer risk through aberrations in DNA synthesis, repair, and methylation.3 Vitamin B6 may also suppress colorectal carcinogenesis by reducing cell proliferation, angiogenesis, oxidative stress, inflammation, and nitric oxide synthesis.4- 6Major food sources of vitamin B6 include fortified cereals, meat, fish, poultry, starchy vegetables, and some fruits (eg, bananas and avocado).1
Findings from prospective studies that have examined the association between vitamin B6 intake or PLP levels in the blood and the risk of colorectal cancer have been inconsistent. The aim of this review was to evaluate the evidence from prospective studies on vitamin B6 intake or blood levels of PLP and the risk of colorectal cancer by summarizing it quantitatively with a meta-analytic approach.