Purpose of review:
We present a current perspective of epigenetic alterations that can lead to cardiovascular disease (CVD)
and the potential of dietary factors to counteract their actions. In addition, we discuss the challenges and
opportunities of dietary treatments as epigenetic modifiers for disease prevention and therapy.
Recent findings:
Recent epigenome-wide association studies along with candidate gene approaches and functional studies
in cell culture and animal models have delineated mechanisms through which nutrients, food compounds
and dietary patterns may affect the epigenome. Several risk factors for CVD, including adiposity,
inflammation and oxidative stress, have been associated with changes in histone acetylation, lower global
DNA methylation levels and shorter telomere length. A surplus of macronutrients such as in a high-fat diet
or deficiencies of specific nutrients such as folate and other B-vitamins can affect the activity of DNA
methyltransferases and histone-modifying enzymes, affecting foetal growth, glucose/lipid metabolism,
oxidative stress, inflammation and atherosclerosis. Bioactive compounds such as polyphenols (resveratrol,
curcumin) or epigallocatechin may activate deacetylases Sirtuins (SIRTs), histone deacetylases or
acetyltransferases and in turn the response of inflammatory mediators. Adherence to cardioprotective
dietary patterns, such as the Mediterranean diet (MedDiet), has been associated with altered methylation
and expression of genes related to inflammation and immuno-competence.
Summary:
The mechanisms through which nutrients and dietary patterns may alter the cardiovascular epigenome
remain elusive. The research challenge is to determine which of these nutriepigenetic effects are rev