Many childhood-onset diseases used to be lethal. Improved life expectancy yield that most patients can survive into adulthood, to date. However, survivors of childhood-onset diseases often develop morbidities that suggest accelerated aging. Congenital heart disease is a typical example of a childhood-onset disease. It is the most common birth defect, comprising a spectrum of mild, moderate and complex heart defects. Several age-related morbidities occur more often and at an earlier age in these patients. The overall goal of this project is to quantify and understand disparities in chronological and biological age over the lifespan in patients with congenital heart disease. We will measure indicators and risk factors for aging over the entire lifespan, from the beginning of life until advanced age. We propose 3 studies, in which we will include 288 newborns and 500 (young) adults with congenital heart disease. As a marker of aging, we will measure the length of telomeres, which are the protective ends of chromosomes. Clinical, behavioral, psychological and social predictors will be scrutinized to investigate how aging can be explained. In a selected group of 200 adult patients, the epigenetic clock based on DNA methylation will be determined. This is a novel technique to assess the disparity between biological and chronological age.