ABSTRACT
The overwhelming body of evidence suggests that environmental factors, including diet, inuence our susceptibility to disease including cancer. Individual variations in disease susceptibility to environmental factors cannot entirely be accounted for by conventional genetic mechanisms. In this regard, epigenetics modications including DNA methylation, histone modications, chromatin remodeling, and RNA interference have emerged as a promising mechanism by which environmental factors including diet can inuence disease susceptibility. In contrast to genetic changes in human diseases, epigenetic changes are gradual in onset and progression and are potentially reversible by dietary and pharmacological manipulations.1 Aberrant patterns and dysregulation of epigenetics play a critical role in the development and progression of cancer including colorectal cancer (CRC).1 Because of the critical role of folate in biological methylation reactions including DNA methylation and a purported relationship between folate status and CRC risk, there has been considerable interest in investigating whether DNA methylation might be a link between folate status and CRC risk.1,2 Given this consideration, the aim of this chapter is to review the currently available evidence for the purported association between folate status and CRC risk and to review whether the modulatory effect of folate on CRC risk is mediated in part through epigenetic modications, in particular alterations in DNA methylation.
