Methyl nutrients, DNA methylation, and cardiovascular disease

Authors

  • Melissa B. Glier,

    1. Department of Pathology and Laboratory Medicine, Child and Family Research Institute, University of British Columbia, Vancouver, Canada
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  • Timothy J. Green,

    1. Department of Food, Nutrition, and Health, Child and Family Research Institute, University of British Columbia, Vancouver, Canada
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  • Angela M. Devlin

    Corresponding author
    1. Department of Pathology and Laboratory Medicine, Child and Family Research Institute, University of British Columbia, Vancouver, Canada
    2. Department of Pediatrics, Child and Family Research Institute, University of British Columbia, Vancouver, Canada
    • Correspondence: Dr. Angela M. Devlin, Department of Pediatrics, University of British Columbia, Child and Family Research Institute, 272–950 West 28th Ave, Vancouver, Canada V5Z 4H4

      E-mail: adevlin@cfri.ubc.ca

      Fax: +1-604-875-3597

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Abstract

Diet plays an important role in the development and prevention of cardiovascular disease (CVD), but the molecular mechanisms are not fully understood. DNA methylation has been implicated as an underlying molecular mechanism that may account for the effect of dietary factors on the development and prevention of CVD. DNA methylation is an epigenetic process that provides “marks” in the genome by which genes are set to be transcriptionally activated or silenced. Epigenomic marks are heritable but are also responsive to environmental shifts, such as changes in nutritional status, and are especially vulnerable during development. S-adenosylmethionine is the methyl group donor for DNA methylation and several nutrients are required for the production of S-adenosylmethionine. These methyl nutrients include vitamins (folate, riboflavin, vitamin B12, vitamin B6, choline) and amino acids (methionine, cysteine, serine, glycine). As such, imbalances in the metabolism of these nutrients have the potential to affect DNA methylation. The focus of this review is to provide an overview on the current understanding of the relationship between methyl nutrient status and DNA methylation patterns and the potential role of this interaction in CVD pathology.

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