User:Rosieohare/sandbox

The TDS hypothesis proposes that testicular dysgenesis, which has numerous genetic and environmental primary causes, can lead to abnormalities in Sertoli and/or Leydig cell function. This leads to both impaired germ cell development and hormonal changes during male sexual differentiation. For instance, insufficient production of testosterone can result in incomplete masculinisation, whilst reduced expression of insulin-like factor 3 can lead to incomplete testes descent (Sharpe & Shakkebaek, 2008). The downstream disorders of such abnormalities can include both genital malformations (e.g. hypospadias and cryptorchidism) and delayed reproductive disorders (e.g. testis cancer and poor semen quality) which comprise TDS. (Bay et al., 2006) (Figure 1).