emerging evidence strongly suggests that consumption of dietary agents can alter normal epigenetic states as well as reverse abnormal gene activation or silencing. It is thus cleas that dietary factors influence the epigenome and could be used in combination with other cancer prevention and chemotherapeutic therapies (Hardy and tollefsbol, 2011). Nutrients involved in one-carbon metabolism, namely folate, vitamin B12, vitamin B6, riboflavin, methionine, choline and betaine, are involved in DNA methylation by regulating levels of the universal methyl donor S-adenosylmethionine and methyltransferase inhibitor S-adenosylhomocysteine (Park, Friso, & Choi, 2012).
While, other nutrients and bioactive food components such as retinoic acid, resveratrol, curcumin, sulforaphane and tea polyphenols can modulate epigenetic patterns by altering the levels of S-adenosylmethionine and S-adenosylhomocysteine or directing the enzymes that catalyse DNA methylation and histone modifications (Park, Friso, & Choi, 2012).
Furthermore, evidence implicate that excessive ethanol ingestion and folate deficiency are identified as risk factors for several cancers. It this clear that ethanol impedes the bioavailability of dietary folate and is known to inhibit select folate-dependent biochemical reactions. In animal models, chronic alcohol ingestion was shown to produce hypomethylation of DNA in the colonic mucosa, a constant feature of early colorectal neoplasia. In addition, alcohol may redirect the utilization of folate toward serine synthesis and thereby may interfere with a critical function of methylenetetrahydrofolate, thymidine synthesis. It is thus clear that there is a significant metabolic association between alcohol and folate metabolism that needs further investigation (Park, Friso, & Choi, 2012).
Park, Friso, & Choi (2012) emphesized that since aging and age-related diseases are associated with profound changes in epigenetic patterns, identification epigenetic pattern that facilitate healthy aging through nutritional measures is crucial.
Recent studies suggest that epigallocatechin-3-gallate (EGCG), which is the main polyphenolic constituent of green tea, may be used for the prevention and treatment of various neurodegenerative diseases by promotes neural progenitor cell proliferation and sonic hedgehog pathway activation during adult hippocampal neurogenesis (Wang, Li, Xu, Song, Tao, & Bai, 2012). These results are suggestive that EGCG may be beneficial to hippocampus-dependent learning and memory.
It is well established that epigenetic modifications is reversible, which makes modulation of epigenetic states a potential new therapeutic option for cancer and other disease (Corpet & Almouzni, 2007). A number of agents that alter patterns of DNA mythelation are being tested in clinical trail (Egger, Liang, Aparicio, and Jone, 2004), along with ongoing research for agents that can inhibit methyltranferases directly to target other epigenetic regulators (Corpet, A., & Almouzni, 2007).