Maternal Factors and the Placenta: A Programming Environment for Cardiovascular Disease

The risk of chronic diseases such as cardiovascular diseases (CVD) during postnatal life is not only determined by environmental factors in adulthood but also by intra-uterine and early life environment according to the Developmental Origins of Health and Disease (DOHaD) concept. Environmental insults including poor nutrition, oxygen availability, maternal stress, alcohol, smoking and drugs, can compromise the maternal uterine and lactational environment leading to short- and long-term adaptations in offspring physiology or programming. While short-term predictive adaptive responses may offer immediate survival value, they can lead to irreversible changes in embryonic/fetal tissues and organs mediated through changes in cellular signalling and metabolic pathways, as well as endocrine axes governing whole-body function. The capacity for developmental adaptation may also be determined by both genetic susceptibility and epigenetic mechanisms, as well as environmentally induced changes in maternal microbiome structure and composition. Basic mechanisms involved in the development of CVD have been described in previous chapters. Here we will focus on how mechanisms involved in developmental programming may contribute to CVD in adulthood.

Keywords: Developmental programming, Epigenetics, Foetal growth, Hormones, Hypoxia, Metabolism, Nitric oxide, Placenta