Epigenetic Mechanisms in Developmental Origin of Health and Disease

The Developmental Origins of Health and Disease (DOHaD) theory states that exposure to environmental factors during fetal development will have short- and long-term consequences in an individual’s health. The Barker’s hypothesis, also referred to as “thrifty phenotype hypothesis”, proposes that poor nutrition during development produces permanent changes in the fetus leading to poor fetal and infant growth and subsequent metabolic syndromes later in life. These earlier observations suggested that early environmental exposures, such as gestational hyperglycemia, maternal obesity and overfeeding during pregnancy, alter the programming of genes resulting in a long-term imprint on gene expression that lasts into adulthood. These long-term effects are now believed to be mediated by epigenetic changes and evidence supportive of such assumptions is emerging. Hence, studies of gestational and neonatal diseases provide an ideal setup to investigate the epigenetic plasticity during development, the interactions with other factors - such as nutrition, microbiome colonization, etc.-, and how such interactions influence the human phenotype postnatally and the epigenetic mechanisms regulating them.

This Collection is dedicated to highlight the most recent advances in epigenetic research pertaining developmental origins of health and disease, including mechanistic, targeted, and genome-wide epigenetic analyses. As such, we invite submission of manuscripts encompassing any studies that are focused on epigenetics in DOHaD to increase our understanding of developmental epigenetic plasticity, how it conditions health postnatally, and the possible translation of this knowledge into clinical practice.