Not only the genome but also the epigenome stores heritable information. The genome is supposed to stay stable during lifetime, while the epigenome is very dynamic and modulated by environmental stimuli, such as dietary molecules. It is expected that the missing classical genetic heritability of the susceptibility for complex diseases and traits might be eventually explainable via epigenetics. For example, persons that are born with low birth weight have a high risk to develop T2D later in their life, suggesting that epigenetic programming during embryogenesis and the intra-uterine environment both contribute to the T2D risk. Moreover, the lifestyle of the human individual, i.e. primarily the daily choice of diet, seems to create a metabolic memory within the epigenome. This concept suggests that lifestyle changes, such as the use of personalized diet, increased physical activity and consecutively weight loss can have a beneficial effect on the epigenome and thus on the risk for suffering from the metabolic syndrome (Chap 12).
In this chapter, we will define different epigenetic mechanisms, such as post-translational histone modifications and DNA methylation, that process information provided by dietary molecules. We will learn that many chromatin-modifying enzymes are susceptible to changes in the levels of intermediary metabolites acting as co-substrates and co-factors and respond to changes in nutrient intake and metabolism. Via the understanding of pre-natal supplementation in mouse models, we will get insight into the concepts of epigenetic programming. This will lead us to the thrifty hypothesis, and we will discuss the different approaches of epigenetic epidemiology including the concept of an “epigenetic drift” during adult life.