An increasing amount of epidemiological and pathological evidence has been provided that indicates that maternal hyperlipidemia during embryonic development is correlated with an increased risk for atherosclerosis in the offspring during adulthood. In utero, the placenta and fetus are exposed to high cholesterol, lipid invasion, oxidative stress, inflammation and immune reaction signals from the mother and will likely respond specifically. In the fetus, these responses may lead to permanent epigenetic changes and these changes may lead to increased atherosclerosis susceptibility in adulthood.