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Hypogonadism in a male refers to a decrease in either of the two major functions of the testes: sperm production or testosterone production. These abnormalities can result from disease of the testes (primary hypogonadism) or disease of the pituitary or hypothalamus (secondary hypogonadism). The use of testosterone to treat hypogonadism in adult men, primary or secondary, is reviewed here. The clinical manifestations and diagnosis of male hypogonadism, induction of spermatogenesis in men with secondary hypogonadism, and induction of puberty with testosterone are discussed elsewhere. (See "Clinical features and diagnosis of male hypogonadism" and "Induction of fertility in men with secondary hypogonadism" and "Diagnosis and treatment of delayed puberty", section on 'Testosterone therapy' .)
The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".   Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.  The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.  Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.