Commentary: The seven plagues of epigenetic epidemiology.

Heijmans BT, Mill J.

Int J Epidemiol. 2012 Feb;41(1):74-8.

Epigenetics is being increasingly combined with epidemiology to add mechanistic understanding to associations observed between environmental, genetic and stochastic factors and human disease phenotypes. Currently, epigenetic epidemiological studies primarily focus on exploring if and where the epigenome (i.e. the overall epigenetic state of a cell) is influenced by specific environmental exposures like prenatal nutrition, sun exposure and smoking. In this issue of the IJE, Nada Borghol et al. report an association between childhood social-economic status (SES) and differential DNA methylation in adulthood. Low SES may integrate diverse and heterogeneous environmental influences, and knowing which epigenetic changes are associated with low SES may provide clues about the biological processes underlying its health consequences. The authors stress that their study is preliminary. This statement is, in fact, to a greater or lesser extent applicable to the entire first wave of studies currently being published that likewise aim to discover associations between epigenetic variation measured on a genome-wide scale and environmental exposures or disease phenotypes. When executing such epigenome-wide association studies (EWASs), every epigenetic epidemiologist is struggling with the same biological, technical and methodological issues. It is important to take these into consideration when designing a study and interpreting the results. Let us consider seven of those issues, taking the current study on SES as a starting point.
<<<<<<< HEAD ======= >>>>>>> Fix publications statics loading