It has been well known for many years that prenatal life is not fully protected in the uterine microenvironment. But only over the last decade we have been focusing on mechanisms and modalities of maternal and foetal exposure to an impressive range of chemicals (e.g.: endocrine disruptors), physical factors (e.g.: ionizing radiations) and biological agents (e.g.: viruses) able to induce potentially adaptive and predictive epigenetic changes in the embryo-fetal genome, thus interfering with the programming of tissues and organs in an often irreversible way. Sometimes these epigenetic marks could be even inherited from one generation to another. This new awareness could radically transform the representation of the individual development (ontogeny) and of the evolution of our species (phylogeny).
This model of pathogenesis is the so-called theory of the embryo-foetal origins of adult diseases (DOHAD: Developmental Origins of Health and Diseases). This new paradigm is important not only to explain in a more exhaustive way the embryo-foetal origins of all the above mentioned disorders and their dramatic increase over the last decades, but also to try to effectively face this epidemiological transition. The key-term in this context is certainly primary prevention: only by reducing the maternal-foetal factors of distress and the exposure of the foetus (and of its gametes) to pollutants, it would be possible to protect the correct programming of cells, tissues and organs.
Proceedings of the 11th International Workshop on Neonatology and Satellite Meetings · Cagliari (Italy) · October 26th-31st, 2015 · From the womb to the adult
Guest Editors: Vassilios Fanos (Cagliari, Italy), Michele Mussap (Genoa, Italy), Antonio Del Vecchio (Bari, Italy), Bo Sun (Shanghai, China), Dorret I. Boomsma (Amsterdam, the Netherlands), Gavino Faa (Cagliari, Italy), Antonio Giordano (Philadelphia, USA)