Epigenetic changes are a strategy enabling the genome to "respond" to changing environmental conditions. Certain genomic regions are especially sensitive to early (critical time window) nutritional influence. For instance, data support the hypothesis that individuals with metabolic syndrome, combining disturbances in glucose and insulin metabolism have suffered improper "epigenetic programming" during their fetal/postnatal development due to maternal inadequate nutrition and metabolic disorders.

Studies on inbred mice in Randy Jirtle's laboratory at the Duke University (USA) demonstrated how changes of the diet (methyl donor-rich supplements such as folic acid and vitamin B12) can effect their offspring. Fur colour turned brown, yellow or mottled depending on how the agouti gene was methylated during embryonic growth, directly correlating with their diet.

In other studies, similar results were obtained testing genistein (a phyto-oestrogen in soy) and polyphenol from green tea. Epidemiologic work shows that prenatal and early postnatal nutrition influence adult susceptibility to diet-related chronic diseases including cardiovascular disease, type 2 diabetes, obesity and cancer. However, epigenetic changes are not limited to early development. Folic acid, betaine, vitamin B12 and zinc play an important role in the synthesis of S-adenosyl methionine (SAM) and thus in mechanisms leading to gene methylation. L-carnitine, on the other hand, is considered to have histone-acytelating effects.
Folate deficiency predisposes to several complex diseases including anaemia, neural tube defects and many types of cancer. Understanding the specific epigenetic mechanisms involved should allow for nutritional interventions, or even corrective therapies using folate, betain, vitamin B12 or zinc.

For example, the risk for liver or colorectal cancer, which is increased by methyl-donor deficiency combined with alcohol consumption and smoking, could be reduced by a diet rich in folate.
Methylenetetrahydrofolate reductase (MTHFR) deficiency is linked to low levels of folic acid, methionine and SAM. Its symptoms can be reduced by intake of betaine as an alternative source of methyl groups for remethylation of homocysteine to methionine. It needs to be mentioned that hyper- as well as hypo-methylation of genes can represent a health risk (see also here).
Additional research is required to further clarify the mechanisms leading to epigenetic changes and to answer the question why some genes are targets for (de-)methylation and others not.

For further reading visit:
Bjornsson HT et al. An integrated epigenetic and genetic approach to common human disease. Trends Genet 2004; 20(8): 350-358.
Dolinoy DC et al. Epigenetic gene regulation: Linking early developmental environment to adult disease. Reprod Toxicol 2006
Junien et al. Nutritional epigenomics of metabolic syndrome, Med Sci (Paris) 2005; 21 Spec No:44-52
Waterland RA and Jirtle RL. Early Nutrition, Epigenetic Changes at Transposons and Imprinted Genes, and Enhances Susceptibility to Adult Chronic Diseases. Nutrition 2004; 20: 63-68
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