Health Professionals:

Research on Folic Acid

A relationship between folate status or intake and several types of cancer, including cancers of the colon, breast, and cervix, have been reported. There are two mechanisms by which folate may modulate cancer risk.

First, folate is needed to form thymine, one of the four deoxynucleotide components of DNA. If folate is in short supply, the base uracil will inappropriately be incorporated into DNA in place of thymine. A DNA correction enzyme will attempt to correct the error by extracting the uracil and inserting a thymine moiety. However, this action can potentially leave nicks in the DNA strand.

If two nicks occur adjacent to each other on DNA strands the DNA could break and become unstable, which could promote carcinogenesis. Folate depletion has been linked to carcinogenesis and is associated with an increased rate of uracil misincorporation into the DNA of humans (Blount et al. 1997, Berger et al. 2008).

The second mechanism involves the process of DNA methylation. Folate is instrumental in producing methyl groups needed to modify DNA. Methylation patterns in DNA help control gene expression. When folate is in short supply, DNA can be undermethylated (hypomethylated) and genes that are normally silenced may be erroneously expressed.

Erroneous expression of a proto-oncogene could initiate a process that leads to carcinogenesis. DNA hypomethylation or other abnormal methylation patterns have commonly been observed in cancerous tissue and DNA hypomethylation has been observed in humans consuming a low folate diet (Jacob et al. 1998, Rampersaud et al. 2000, Bailey et al. 2015).