The natural history of metabolic syndrome and polycystic ovary syndrome (PCOS), which shares many components of metabolic syndrome, may originate in intrauterine life. Evidence from epidemiological observations, clinical, and experimental animal studies suggest that the nutritional, hormonal, and metabolic environment afforded by the mother may permanently program differentiating target tissues of the offspring toward the development of metabolic syndrome/PCOS phenotype in adult life. The mechanisms of fetal programming are not well understood. Thus, the altered tissue differentiation may be the result of fetal adaptive responses representing homeostatic adaptations due to alterations in fetal nutrition. Also, tissues under the influence of androgen excess may be directed toward a more masculine phenotype with regard to reproductive, neuroendocrine, and metabolic traits, while the importance of epigenetics in fetal origin of metabolic syndrome/PCOS cannot be overlooked.