Adult risk factors such as tobacco

Possibly ensuing an ‘epigenetic diet’, various dietary bioactive food components have been observed to alter gene expression via changes in DNA methylation [32] and [68]. The availability of the methyl-donor, S-adenosylmethionine (SAM) is determined by one-carbon metabolism. This is a pathway that involves vitamins B6 and B12, betaine, folate and choline as well as various BMS-708163 such as glycine, methionine, serine and cysteine. If a component of the pathway is missing, such as deficiency in B vitamins, DNA methylation is altered [65]. In addition to altering availability of B vitamins, alcohol consumption causes wastage of choline and methionine, reducing the amount of SAM available and thereby altering DNA methylation [59] and [88]. The diet is found to be an imperative determinant in the manifestation of late-onset disease. Vitamins and folates influence activity of enzymes that partake in cellular methylation processes and very much influence the rate of disease symptoms. Genomic instability and hypomethylation is allied with reduced amounts of folates [40] and [41]. In mice, increased intake of folic acid increased DNA methylation of an allele in the coat colour agouti locus, resulting in gene silencing and phenotypic modifications [99] and [90]. Additionally, methyl-deficient diets induce liver cancers associated with hypomethylation and enhanced expression of oncogenes such as c-fos and c-ras [25] and [41].