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
