Causes of transsexuality Docter and others, but opposed by Charles Allen Moser, Larry Nuttbrock, Julia Serano, and the World Professional Association for Transgender Health.<section end="factors" /> A 2008 study compared 112 male-to-female transsexuals (both androphilic and gynephilic), mostly already undergoing hormone treatment, with 258 cisgender male controls. Male-to-female transsexuals were more likely than cisgender males to have a longer version of a receptor gene (longer repetitions of the gene) for the sex hormone androgen or testosterone, which reduced its effectiveness at binding testosterone. The androgen receptor (NR3C4) is activated by the binding of testosterone or dihydrotestosterone, where it plays a critical role in
Familial male-limited precocious puberty Familial male-limited precocious puberty Familial male-limited precocious puberty, often abbreviated as FMPP, also known as familial sexual precocity or gonadotropin-independent testotoxicosis, is a form of gonadotropin-independent precocious puberty in which boys experience early onset and progression of puberty. Signs of puberty can develop as early as an age of 1 year. The spinal length in boys may be short due to a rapid advance in epiphyseal maturation. It is an autosomal dominant condition with a mutation of the luteinizing hormone (LH) receptor. Treatment is with drugs that suppress gonadal steroidogenesis, such as cyproterone acetate, ketoconazole, spironolactone, and testolactone. Alternatively, the