Article

Nutritional influences on epigenetics and age-related disease

Vitamins and Carcinogenesis Laboratory, Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
Proceedings of The Nutrition Society (Impact Factor: 5.27). 11/2011; 71(1):75-83. DOI: 10.1017/S0029665111003302
Source: PubMed

ABSTRACT

Nutritional epigenetics has emerged as a novel mechanism underlying gene-diet interactions, further elucidating the modulatory role of nutrition in aging and age-related disease development. Epigenetics is defined as a heritable modification to the DNA that regulates chromosome architecture and modulates gene expression without changes in the underlying bp sequence, ultimately determining phenotype from genotype. DNA methylation and post-translational histone modifications are classical levels of epigenetic regulation. Epigenetic phenomena are critical from embryonic development through the aging process, with aberrations in epigenetic patterns emerging as aetiological mechanisms in many age-related diseases such as cancer, CVD and neurodegenerative disorders. Nutrients can act as the source of epigenetic modifications and can regulate the placement of these modifications. 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. 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. Aging and age-related diseases are associated with profound changes in epigenetic patterns, though it is not yet known whether these changes are programmatic or stochastic in nature. Future work in this field seeks to characterise the epigenetic pattern of healthy aging to ultimately identify nutritional measures to achieve this pattern.

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    • "Since MS activity determines the ratio of the methyl donor S-adenosylmethionine (SAM) to the endogenous methylation inhibitor S-adenosylhomocysteine (SAH), MeCbl is poised to influence hundreds of SAM-dependent methylation reactions, affecting nearly every aspect of metabolism. Important among these reactions is methylation of DNA and histones, which combine to exert dynamic epigenetic control over gene expression[3]. MeCbl is also required for dopamine-stimulated phospholipid methylation, a unique activity of D4 dopamine receptors[4], which depends upon MS activity[5]and has been proposed to play an important role in neuronal synchronization and attention[6]. "
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    Full-text · Article · Jan 2016 · PLoS ONE
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    Full-text · Article · Sep 2015 · Andrologia
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    • "Similarly, deficiency of B vitamins, methionine, folic acid and/or choline can significantly alter DNA methylation by affecting levels of SAM and SAH [21] [22]. However, while these studies indicate the interaction between nutrients and the pathways regulating DNA methylation, it is still unclear how a specific gene is targeted by nutrients or alternatively, if these changes are stochastic in nature [21] [23]. "
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