Abstract
While it takes years for the morphological changes of atherosclerosis to develop and become manifest as clinical cardiovascular (CV) disease in middle age (1,2), origins of the disease may track from fetal life. Epidemiological evidence and animal studies implicate exposures in fetal life as determinants of obesity, Type 2 diabetes, and other CV risk factors that stimulate atherogenic processes leading to CV disease. Maternal health and nutrition during pregnancy and fetal growth and well-being may influence metabolic programming in the fetus, setting a trajectory culminating in the development of CV risk factors and ultimately CV disease. For prevention of CV disease future research must define the prevention strategies that can be implemented early in life and continue throughout the life-course. © 2010 Blackwell Publishing Ltd.