Cardiovascular disease (CVD) is a leading cause of mortality and is projected to hold its grim record as developing countries increase their wealth. Since specific nutritional habits are important risk factors for CVD, it is imperative to understand how ingredients of risk-associated diets convert a healthy cellular transcriptional program into a pathological one. Epigenetics has enriched our view of the genome by showing that DNA-associated regulatory proteins and RNAs, together with chemical modifications of the DNA itself, determine which parts of the DNA chain are transcribed or silent in a given phase of a cell's life. This complex biological entity--the epigenome--accounts for the enormous phenotypic diversity within a multicellular organism despite its unicellular origin. Crucially, the epigenome can be modified by diet and other exogenous factors, thus suggesting that epigenetic mechanisms might underlie pathological responses to CVD risk factors. Here, we will review the current knowledge of epigenetic mechanisms in diet-gene interactions and propose ways in which epigenetics might clarify the impact of genetic variants on CVD risk.