Severe childhood adversity is thought to be one of the strongest risk factors for three major public health problems: cardiovascular disease, upper respiratory tract infections (URTI) and mental health problems. The three disease groups have all been linked to changes in how our body responds to stress. The main stress response system, the hypothalamus-pituitary-adrenal (HPA) axis, is conditioned by the environment, particularly during early life.The principal interface between the environment and the genome is epigenetic methylation of genomic DNA. There is a clear link between adverse early life experiences and disregulation of the HPA axis by epigenetic DNA methylation. The associated pathologies such as cardiovascular diseases and mental health problems have also been associated with epigenetic alterations. Our working hypothesis is that early life adversity induces high risk epigenetic modifications for the above disorders. We suggest that genome wide epigenetic modifications, implicated in all three of the above disease groups, have a common early life origin. This will be investigated in a cohort of young adults. It is also envisaged that the cohort will be maintained for follow-up studies of EpiPath and others. It can be anticipated that in future projects the prognostic and diagnostic value of the epigenetic marks identified in this project will be reexamined both as biomarkers of ELA and as risk factors for later-life pathologies.