Epigenetics and DOHaD: from basics to birth and beyond

J Dev Orig Health Dis. 2017 Oct;8(5):513-519. doi: 10.1017/S2040174417000733. Epub 2017 Sep 11.


Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

Keywords: animal models; diet; epigenetics; metabolic health; microbiome.

Publication types

  • Review

MeSH terms

  • Animals
  • DNA Methylation / physiology
  • Environmental Exposure / adverse effects*
  • Epigenesis, Genetic / physiology*
  • Feeding Behavior / physiology
  • Female
  • Gastrointestinal Microbiome / physiology*
  • Health Status*
  • Humans
  • Pregnancy
  • Prenatal Exposure Delayed Effects / genetics*
  • Prenatal Exposure Delayed Effects / metabolism