The hypothesis that malformations of the male reproductive organs along with impaired semen quality, reduced testosterone production and testicular germ cell cancer, constitute a syndrome of testicular dysgenesis (TDS) with a common origin in fetal life, was put forward by researchers from the department in 2001.
The TDS hypothesis is now well established and used as a working hypothesis in labs throughout the world.
According to the TDS hypothesis, intrauterine growth disorders, genetic defects or polymorphisms, inappropriate lifestyle of the pregnant mother or exposure to harmful environmental factors in fetal life, may disturb the normal genesis of the testis. This may result in effects which are apparent already at birth, as for example cryptorchidism or hypospadias, or only manifest in adulthood, like poor semen quality or development of testicular cancer.
In order to investigate TDS in humans, a large mother-child cohort has been established and followed up by researchers in the department. Questionnaire data, hormone profiles, careful clinical examination data and chemical analysis data of exposure to various endocrine disrupters are collected in large and complex data sets, which are still increasing in size, as the children are now followed up during their pubertal years. Hopefully, these data may give us a clue on which factors may lead to TDS.