Presenter
Umberto Simeoni
Umberto Simeoniās research explores how child development interacts with the environment, helping uncover the biological roots of adult health and disease. He has held professorships in pediatrics at Louis Pasteur University and University Hospital of Strasbourg, Aix-Marseille University and AP-HM University Hospital (where he led the Parents-Children Department), and currently at Lausanne University Hospital and University of Lausanne, where he directs the DOHaD* research lab. His clinical focus includes neonatal and perinatal medicine, child development, and perinatal bioethics. He has authored numerous peer-reviewed publications and delivered invited lectures internationally. Simeoni has served as president or board member of the European Association for Perinatal Medicine, the Francophone Association for Neonatal Research, the French Perinatal Society, and the Francophone DOHaD Society, which he co-founded. He also co-founded Fertil-In, which promotes reproductive and transgenerational health.
Abstract:
Epidemiological and biological data show that while an organism develops based on its genome, it is especially shaped by sustained interactions with its environment. This developmental plasticity allows a single genotype to yield a range of phenotypes, seemingly following a predictive model: early-life environmental signals can have lasting effects, while the same signals later are often transient. In humans, factors during the periconceptional period, pregnancy, and early childhoodāsuch as nutrition, lifestyle, and exposure to toxins or stressācan program the development of key biological systems. A mismatch between early-life predictions and later environments can contribute to chronic diseases like obesity, diabetes, cardiovascular disorders, and accelerated aging. Epigenetic mechanismsāincluding DNA methylation, histone modifications, and non-coding RNAsāmediate genome-environment interaction and support long-term programming. Early stress, especially oxidative stress, may accelerate cellular senescence via epigenetic changes in pathways like sirtuin 1, forming a common mechanism in altered developmental trajectories. These effects appear across species and systems. Epigenetic marks may be transmitted across generations, amplifying the impact of developmental programming. Shifts in behavior and lifestyle, shaped by early programming, could help explain the global rise in chronic disease. A life courseāor life cycleāapproach to health and aging supports prevention-focused health policies. Current priorities include reprogramming through personalized education and support, especially targeting young adults planning families. e-Health and m-Health tools offer promise. Epigenetics may also provide early biomarkers and therapeutic targets to detect and reverse chronic disease risk.
