In utero exposure and endometriosis

Abstract

Adverse living and nutritional conditions in utero and in early infancy may influence the risk of diseases in adult life, because fetal growth seems determined by interactions between the environment and the fetal genome and these interactions may determine the risk of postnatal disease and the capacity to react to and cope with the postnatal environment. It has been proven that massive fetal exposure to toxic agents causes an increased incidence of negative outcomes in pregnant women; of particular interest is the association between in utero exposure to toxic agents and the occurrence of endometriosis. There is evidence that exposure to dioxins can facilitate short-term survival of endometrial implants in non-human primates, but there is no solid evidence that it may lead to endometriosis in humans. In the case of diethylstilbestrol, an increased risk of developing endometriosis seems well established, although the mechanisms through which diethylstilbestrol can modify endometrial physiology remain uncertain. Finally, evidence that environmental and specific dietary factors may play a role in increasing the incidence of endometriosis and other pathologic conditions has accumulated over the years. Although the hypothesis may be valid, the most recent investigations have failed to find specific, significant correlations.

• Endocrine-disrupting chemicals
• endometriosis
• environmental toxins
• reproduction