This project investigates the evolutionary history of cardiogenesis and its implications for con- genital heart diseases (CHD) in humans, applying principles from evolutionary medicine to deepen our understanding of the origins and mechanisms underlying these conditions. While some CHDs are linked to identifiable genetic defects, the majority arise from non-genetic fac- tors, such as environmental influences, which disrupt the development of the outflow tract (OFT) of the heart. This project explores the hypothesis that the same evolutionary mecha- nisms that allowed for key innovations in vertebrate OFT evolution may also contribute to the susceptibility of human cardiogenesis to malformations.

I propose the Environmentally Dependent Developmental Induction model, which posits that environmental changes during key developmental stages can induce phenotypic changes without relying solely on genetic mutations. This model emphasizes the importance of extrinsic factors, such as oxygen levels, in shaping cardiac development. Experiments with chick embryos support the hypothesis that reduced oxygen availability during critical periods inhibits apoptosis in the OFT, leading to malformations similar to severe CHD in humans.

By bridging evolutionary biology and clinical research, this work aims to provide a deeper understanding of the evolutionary mechanisms underlying CHD, with potential applications in improving diagnostic tools, preventative measures, and treatment strategies. The interdisciplinary approach of this research makes it relevant to a broad audience, including evolutionary biologists, geneticists, developmental biologists, and medical professionals, particularly those specializing in cardiology.