Various hypotheses as to the origin of preeclampsia have been explored over time. Diseases of pregnancy are difficult to study for several reasons. One limitation is due to the fact that preeclampsia and associated diseases clinically present in the second and third trimenon, but seem to originate early in pregnancy. Comparisons with animal models are difficult due to the unique human nature of the disease. The creation of new methods including proteomics, genomics, lipidomics, metabolomics or mRNA microarray techniques supplement the traditional type of research access to approach mother and fetus. The clinical course will be discussed and pregnancy-related processes, which are thought to contribute to the disease. This includes implantation of the placenta/fetus, the adaptation of the endothelial activity to the pregnancy with respect to relaxin, matrix metalloproteinases and endothelin, nitric oxide, angiogenetic factors and TGF-b in normal and preeclamptic pregnancies. Furthermore, oxidative stress, genetics and hypothesis-generating molecular approaches are considered.