An overwhelming body of evidence links fetal (mal)nutrition to the development of chronic diseases at adult age (DOHaD hypothesis, Developmental Origins of Health and Disease). Several explanations for the various observed facets of the long-term consequences of fetal (under)nutrition are currently under investigation. In recent papers, epigenetic mechanisms like DNA methylation or histone modifications have been proposed to be involved in metabolic programming: CpG islands, CG-dinucleotide-rich regions in the promoter of a gene, have been shown to be of crucial importance for the transcriptional activity of particular promoters. In general, transcription of a gene is blocked when the CpG island is methylated. A second layer of complexity is added by the fact that methylated areas of DNA attract methyl-DNA binding proteins and acquire histone modifications which also affect the accessibility of the DNA for transcription. Together, the interaction of DNA methylation and histone modification can regulate the activity of a DNA region. New technologies (pyrosequencing, next generation sequencing) now enable us to measure DNA methylation and the active/silent areas of chromatin in a genome-wide way and correlate it with physiological observations. Embryonic development proceeds as a complex set of interdependent and precisely integrated biological programmes, initiated by selective transcription of specific genes at specific points of time and regulated by a controlled maternal supply of nutrients. With the current state of knowledge of molecular regulation of cholesterol and lipid metabolism, it is possible to generate a network of metabolic events in the embryo and the fetus that may underlie programming. Nuclear receptors (PPARs, LXRs, FXR) provide the vehicles through which nutrients interact with the (epi)genome. Expression of these nuclear receptors is at least partially under control of CpG islands. Disturbances in this complex network of interactions represent key events in metabolic programming of insulin resistance, hyperlipidemia and cardiovascular disease and are the focus of my work. I will discuss some of the early epigenetic modifications we observed in animal models and human samples and try to link them to metabolic and cardiovascular disease in later life.