Nutrigenetics are the fixed genetic variation (genotype) in response to diet whereas nutrigenomics describes the influence of specific nutrients on gene expression. The unravelling of the human genome had led to hopes that individual susceptibility to major risk factors (blood pressure, lipids, inflammatory and haemostatic factors) might lead to the personalised nutritional advice to avoid cardiovascular disease (CVD). The major problem is that dietary effects are difficult to detect in the first place and diet x genotype interactions are even more so. While relatively common mutations in the low density lipoprotein (LDL) receptor increase by 25 fold the risk of premature CVD, common polymorphisms have much milder effects. Generally, the environmental effects (smoking, physical activity, diet and obesity) overwhelm genetic effects with regard to risk of CVD. Polymorphisms that raise LDL cholesterol are associated with increased risk of CVD. The polymorphism in the apolipoprotein E phenotype is a good example of how individuals differ in their LDL cholesterol response to dietary cholesterol. Polymorphism in the angiotensinogen gene AGT may explain some of the variability in response to diet and blood pressure. Dietary folate and vitamin B12 intake can influence DNA methylation and are potential candidates for explaining the nutrigenomic effects of how maternal diet can affect the outcome of the offspring. The potential nutrigenomic mechanisms by which early diet and development might affect cardiovascular function, particularly blood pressure and risk of type 2 diabetes which both increase risk of CVD in later life, will be discussed.