Abstract
DOHaD research has mainly focused on prenatal maternal factors, although there exist paternal origins of health and disease (POHaD) of the next generation. For example, paternal aging is a risk for autism spectrum disorder (ASD) and low birthweight. In these decades, the number of ASD patients has increased as the age of marriage has shifted. Epidemiological studies repeatedly show that paternal aging matters more on the risk of ASD than maternal aging. Spermatogenesis, in which sperm stem cells divides to make numerous sperm cells, may be more sensitive to genetic mutations and epigenomic changes owing to age than oocytes. There are clinical and basic evidence that epigenomic changes like DNA methylation may increase child risk of neurodevelopmental disorders. In addition, changes in histone modifications and in non-coding RNAs have been observed due to paternal aging. When the molecular mechanisms that cause disease risk in the male germline and how they interact are found, new ways to treat and prevent diseases are likely to be created. This review introduces the epigenomic changes that can occur in the germline, with a particular focus on paternal aging.
