Nutritional Epigenetics

  • Carsten Carlberg
  • Stine Marie Ulven
  • Ferdinand Molnár


In this chapter, we will present nutritional epigenetics as a subdiscipline of nutrigenomics and describe how dietary compounds affect our epigenome. Different epigenetic mechanisms, such as post-translational histone modifications and DNA methylation, process information provided by dietary molecules. Accordingly, many chromatin modifiers use intermediary metabolites, such as acetyl-CoA, α-ketoglutarate, NAD+ or ATP, as co-substrates and/or co-factors. Thus, these enzymes act as sensors for the nutritional status of our tissues and cell types leaving respective marks on their epigenome. Prenatal supplementation in mice as well as natural human experiments provide insight into the concepts of epigenetic programming during embryogenesis and epigenetic drift during adult life. This may explain some of the susceptibility for complex metabolic diseases, such as T2D.


Epigenome Chromatin DNA methylation Histone modifications Chromatin modifiers Intermediary metabolism Acetyl-CoA NAD+ Folate Methylenetetrahydrofolate reductase Agouti mice Epigenetic programming Epigenetic epidemiology Epigenetic drift 

Additional Readings

  1. Barres R, Zierath JR (2016) The role of diet and exercise in the transgenerational epigenetic landscape of T2DM. Nat Rev Endocrinol 12:441–451CrossRefGoogle Scholar
  2. Carlberg, C., and Molnár, F. (2018). Human epigenomics. Springer Textbook Springer. ISBN: 978-981-10-7614-8CrossRefGoogle Scholar
  3. Gut P, Verdin E (2013) The nexus of chromatin regulation and intermediary metabolism. Nature 502:489–498CrossRefGoogle Scholar
  4. Heard E, Martienssen RA (2014) Transgenerational epigenetic inheritance: myths and mechanisms. Cell 157:95–109CrossRefGoogle Scholar
  5. Kinnaird A, Zhao S, Wellen KE, Michelakis ED (2016) Metabolic control of epigenetics in cancer. Nat Rev Cancer 16:694–707CrossRefGoogle Scholar
  6. Sales VM, Ferguson-Smith AC, Patti ME (2017) Epigenetic mechanisms of transmission of metabolic disease across generations. Cell Metab 25:559–571CrossRefGoogle Scholar

Copyright information

© Springer Nature Switzerland AG 2020

Authors and Affiliations

  • Carsten Carlberg
    • 1
  • Stine Marie Ulven
    • 2
  • Ferdinand Molnár
    • 3
  1. 1.Institute of BiomedicineUniversity of Eastern FinlandKuopioFinland
  2. 2.Department of NutritionUniversity of OsloOsloNorway
  3. 3.Department of BiologyNazarbayev UniversityNur-SultanKazakhstan

Personalised recommendations