ABSTRACT
Humans are constantly exposed to environmental factors that have the potential for altering the epigenome and, thus, for changing an individual’s disease risk. Frequently, these factors affect only small subgroups in the general population and exposure is limited to short periods, for example, in the treatment of cancer patients with the histone deacetylase (HDAC) inhibitor belinostat (Ma et al. 2010), or these factors depend on lifestyle choices such as smoking (Launay et al. 2009). This is not the case for human nutrition, including dietary vitamins. The dietary intake of essential nutrients and bioactive food compounds is a process that occurs on a daily basis for the entire life span and, therefore, has great potential for causing changes in the epigenome. Well-documented examples include feeding studies of diets dened by the content of folate, methionine, and possibly choline in agouti mice, where a depletion of multiple methyl donors causes de-repression of a long-terminal repeat in the Avy locus (Cooney et al. 2002; Dolinoy et al. 2006; Waterland and Jirtle 2003; Wolff et al. 1998). Importantly, epidemiologic studies suggest that adult disease risk is associated with poor nutritional status early in development: individuals exposed to famine during the Dutch Hunger Winter in 1944/1945 are the most widely recognized example (Heijmans et al. 2008). Severe starvation of pregnant women in the Dutch Hunger Winter elicited transgenerational effects, that is, an increased disease risk of the unborn child later in life. It remains to be seen whether such scenarios hold true under conditions that are more moderate than the Dutch Hunger Winter.
