
Studies have shown that maternal dietary changes in one-carbon availability (as a cocktail of one-carbon sources) can affect the DNA methylation patterns and phenotype of the offspring as best described in the agouti mouse model ( 18, 19). In addition, environmental exposure to air pollution in general, particulates in air, and benzene have also been linked to changes in DNA methylation and adverse outcomes such as cancer initiation or progression ( 12–17). A change to this patterning during early development would be propagated to all of the cell's descendants and may affect long-term health and development because aberrant DNA methylation is a hallmark of cancer and other disease processes ( 3, 4, 10, 11).ĭNA methylation patterns vary between sexes and change across the life course ( 12–17).

Methylation of genomic DNA modifies gene expression and provides a mechanism for transmitting and perpetuating epigenetic information through DNA replication and cell division across the life span and even transgenerationally ( 8, 9). In the early embryo, DNA methylation patterns are erased and reset across most of the epigenome ( 4–7). The availability of methyl groups to methylate DNA during early embryogenesis can be critical for fetal programming and long-term disease susceptibility ( 4). DNA methylation regulates gene expression, imprinting, and developmental gene regulation ( 1–4). Folic acid, DNA methylation, epigenetic, periconceptional, adolescents, pregnancy, dietary supplements Introductionįolic acid is a form of folate (vitamin B-9), which is a key source of the one-carbon group that methylates DNA, RNA, and proteins.
