Introduction There are sex differences in the incidence of many neuropsychiatric disorders. For example, neurodevelopmental disorders (e.g., autism, attention deficit hyperactivity disorder) and alcohol dependence occur more commonly in males, whereas the incidence of Alzheimer’s disease, anxiety disorders and depression is increased in females. The biological basis for these gender differences is still poorly understood but probably involves a complex interaction between genes, the environment and hormones on the brain across the lifespan. The aim of this chapter is to offer examples of clinical conditions in women where the link between psychopathology and hormonal changes are more clearly supported by the scientific evidence. Within this context, we shall also discuss how hormonal changes occurring during pregnancy are relevant not only for women’s psychopathology but also for the transmission of psychopathology from one generation to the next. The in utero environment Sex hormones: Sex is defined by an individual’s karyotype, which can be either XY (male) or XX (female). This chromosomal difference leads to differentiation of gonads into testes or ovaries, and associated changes in the hormonal milieu of the in utero environment. Human studies have reported a surge of testosterone from the fetal testes, at around the 6th week of pregnancy (Hughes, 2001), peaking between 12 and 18 weeks gestation (Finegan et al., 1989). This results in levels of testosterone at term that are 10 times higher than in females (de Zegher et al., 1992). In males, a second testosterone surge also occurs in the first 3 months after birth (Quigley, 2002). Recent studies suggest that the early testosterone peak(s) plays a significant role in subsequent sex differences in behavioral phenotype and may predispose to sex differences in vulnerability to specific disorders, such as autism (Phoenix et al., 1959). The in utero effects of testosterone exposure on neurotypical human brain development have been investigated in several ways. Studies in females with congenital adrenal hyperplasia (CAH), for example, have reported increased male-typical play behavior in childhood (Hines et al., 2004) and more aggression in adolescence and adulthood (Berenbaum and Resnick, 1997). Increased aggression has also been reported in girls of opposite, compared to same, sex twins (Cohen-Bendahan et al., 2005). In both cases, this has been attributed to increased testosterone exposure prenatally. A further approach has been to examine directly the relationship between fetal testosterone levels measured at amniocentesis and later behavior.