In an article that appeared in Gastroenterology ( 2003 ) researchers at King’s College London demonstrated that low folate status and DNA hypomethylation are associated with colorectal neoplasia.

They assessed the influence of folate status, DNA methylation, and polymorphisms of methylenetetrahydrofolate reductase ( MTHFR 677C-->T and 1298A-->C ), methionine synthase ( MS 2756A-->G ), and cystathionine-beta-synthase ( CBS 844ins68 ) on risk for developing colorectal neoplasia.

Thirty-five patients with adenoma, 28 patients with cancer, and 76 controls were recruited for a case control study.

Cancer patients had 26% lower folate status and 21% lower serum vitamin B 12 concentration compared with controls.
[(3)H] methyl incorporation into colonic DNA was 26% higher in patients with adenoma and 30% higher in patients with cancer compared with controls.

High folate status was associated with decreased risk for cancer.

Colonic and leukocyte DNA hypomethylation were associated with increased risk for adenoma and a nonsignificantly increased risk for cancer.

These same researchers tested the hypothesis that folic acid supplementation increases DNA methylation in leucocytes and colorectal mucosa in patients with colorectal adenoma.

A total of 31 patients were randomised to receive either 400 µg/day folic acid supplement ( n = 15 ) or placebo ( n = 16 ) for 10 weeks.

Folic acid supplementation increased serum and erythrocyte folate concentrations by 81% and 57% respectively, and decreased plasma homocysteine concentration by 12%.

Folic acid supplementation resulted in increases in DNA methylation of 31% in leucocytes and 25% in colonic mucosa.

Source: Gut, 2005


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