Cardiovascular disease is the chief cause of death in Europe and the USA. Most heart attacks are secondary to atherosclerosis, a disease characterised by local thickening of the vessel wall. In the human baby, aortic thickening has been linked with intrauterine growth retardation, suggesting a developmental origin of cardiovascular disease. Genes and nutrition control fetal growth and contribute to the risk of cardiovascular disease in later life, but whether changes in oxygenation during development trigger early origins of disease remains unknown. We investigated the role of oxygen in fetal growth and the origins of cardiovascular disease in the chick embryo. Fertilised eggs were incubated either at sea level or high altitude with and without oxygen supplementation. The chick embryos underwent biometry and aortic wall:lumen area ratio was calculated. Chick embryos incubated at high altitude were hypoxic, growth retarded and had aortic thickening relative to incubations at sea level or at high altitude with oxygen supplementation. We show that developmental hypoxia is an important mechanism determining reduced fetal growth and early origins of cardiovascular disease.