Disturbed sexual differentiation could in some cases be caused by fetal DES exposure
1998 Study Abstract
Male sexual differentiation is dependent on normal testicular function, including secretion of testosterone from the Leydig cells, and müllerian-inhibiting substance from the Sertoli cells.
Sexual differentiation and environmental endocrine disrupters, US National Library of Medicine National Institutes of Health, Bailliere’s clinical endocrinology and metabolism, NCBI PubMed PMID: 9890066, 1998 Apr.
Disturbed image credit aphotoshooter.
External factors, such as anti-androgens and oestrogens, that disturb endocrine balance cause demasculinizing and feminizing effects in the developing male fetus. Oestrogens also causes adverse effects in female fetuses, whereas anti-androgens have little influence.
A growing number of chemicals have been found to possess either weak oestrogenic, anti-androgenic or other hormonal activities, and these are often referred to as endocrine disrupters.
In animals in the wild, abnormal sexual development has been associated with exposure to mixtures of endocrine disrupters. The emerging adverse trends in human reproductive health, such as increased incidences of cryptorchidism, hypospadias and testicular cancer, and the ubiquitous presence of endocrine disrupters in the environment, support the hypothesis that disturbed sexual differentiation could in some cases be caused by increased exposure to environmental endocrine disrupters.